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Sepsis is a heterogeneous syndrome. It is caused by infections, attributing to immune dysfunction pathologically. The disease is characterized by macrophage-mediated inflammation and immune response throughout its development. During septic development, macrophages metabolize crucially with glycolysis remarkably enhanced. The glycolystic enhancement facilitates septic development by promoting the inflammatory response of macrophages and altering their phenotype. Therefore, direct or indirect inhibition of macrophagic glycolysis can alleviate sepsis and neutralize damages to organs functionally, promoting the polarization of anti-inflammatory phenotype. In this review, we aim to investigate the relationship between macrophagic glycolysis and sepsis, focusing on researching into relevant molecular mechanisms by which glycolysis is regulated for treating sepsis. It is concluded that interfering with macrophagic glycolysis may serve as a novel therapeutic strategy for treating sepsis. [ABSTRACT FROM AUTHOR]

Copyright of Shipin Kexue/ Food Science is the property of Food Science Editorial Department and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Background and purpose: Rectal cancer occurs on the inner wall of the rectum, and metastasis-associated in colon cancer 1 (MACC1) can promote drug resistance in colon cancer cells. This study aimed to investigate the effect of MACC1 on oxaliplatin resistance in rectal cancer and its mechanism. Methods: Biosignal analysis of MACC1 and TCF7 expressions in rectal cancer tissues and signaling pathways enriched for MACC1 were carried out. The expressions of MACC1 and TCF7 in rectal cancer cells and rectal cancer oxaliplatin-resistant cells were detected by real-time fluorescence quantitative polymerase chain reaction (RTFQ-PCR), cell viability was detected by cell counting kit-8 (CCK-8), and cell proliferation was detected by cell colony formation assay. ECAR values, lactate production and glucose consumption were detected by Seahorse Biosciences XF96. Western blot was used to detect the expressions of glycolysis-related proteins. Dual luciferase reporter gene and ChIP were used to validate the regulatory relationship between MACC1 and TCF7. Normality test and homogeneity of variance analysis was performed on the data of each group by GraphPad Prism 8.0. If it conformed to normal distribution, one-way ANOVA or t-test would be used for inter group comparison, otherwise the comparison between groups would be conducted using Wilcoxon rank sum test. Using a two-sided test, P<0.05 was considered statistically significant. Results: MACC1 and TCF7 expressions were upregulated in rectal cancer, and knockdown of MACC1 significantly inhibited the viability of rectal cancer drug-resistant cells and the IC50 values of different concentrations of oxaliplatin treatments, as well as reduced the proliferation ability of rectal cancer oxaliplatin-resistant cells. Overexpression of MACC1 was able to promote the proliferation and glycolytic capacity of rectal cancer cells. Further studies revealed that the transcription factor TCF7 existed in the upper reaches of MACC1. Besides, this study analyzed the data from Cancer Genome Atlas Program (TCGA), and the result showed that knockdown of TCF7 was able to attenuate the promotional effect of overexpression of MACC1 on the glycolytic capacity and oxaliplatin resistance of rectal cancer cells. Conclusion: This study demonstrated that the TCF7/MACC1 axis could promote aerobic glycolysis and thus oxaliplatin resistance in rectal cancer cells. The findings suggest that targeting the TCF7/MACC1 axis or inhibiting the aerobic glycolysis pathway may be a novel therapeutic approach to inhibit oxaliplatin resistance in rectal cancer. [ABSTRACT FROM AUTHOR]

Metabolic reprogramming is one of the significant characteristics of malignant tumor development. It provides the tumor with sufficient energy and materials. During the process by which tumor cells acquire metabolic reprogramming, epigenetic changes play a crucial role. N6-methyladenosine (m6A) in mRNA is the most common post-transcriptional modification of mRNA. It regulates the transcription, maturation, translation, and degradation of mRNA. Studies have shown that m6A helps promote the metabolic reprogramming of tumor cells. However, the complete mechanism still requires further research. METTL3 is a key enzyme for m6A methylation that catalyzes m6A progression by forming complexes with other proteins, such as METTL14 and WTAP. Notably, the critical role of METTL3 in the metabolic transition of gastrointestinal tumors has not been given due attention. This article summarizes the specific pathways through which METTL3 affects the reprogramming of cellular glucose metabolism in gastrointestinal tumors. We aimed to clarify the importance of METTL3 in the energy reprogramming of gastrointestinal tumors. [ABSTRACT FROM AUTHOR]

Copyright of Science & Technology of Food Industry is the property of Science & Technology of Food Industry Editorial Office and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Shipin Kexue/ Food Science is the property of Food Science Editorial Department and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Metabolic reprogramming is one of the significant characteristics of malignant tumor development. It provides the tumor with sufficient energy and materials. During the process by which tumor cells acquire metabolic reprogramming, epigenetic changes play a crucial role. N6-methyladenosine (m6A) in mRNA is the most common post-transcriptional modification of mRNA. It regulates the transcription, maturation, translation, and degradation of mRNA. Studies have shown that m6A helps promote the metabolic reprogramming of tumor cells. However, the complete mechanism still requires further research. METTL3 is a key enzyme for m6A methylation that catalyzes m6A progression by forming complexes with other proteins, such as METTL14 and WTAP. Notably, the critical role of METTL3 in the metabolic transition of gastrointestinal tumors has not been given due attention. This article summarizes the specific pathways through which METTL3 affects the reprogramming of cellular glucose metabolism in gastrointestinal tumors. We aimed to clarify the importance of METTL3 in the energy reprogramming of gastrointestinal tumors.

The postmortem conversion of muscle to meat goes through a series of complex physiological and biochemical changes, among which protein post-translational modifications (PTMs) are key factors affecting meat quality. Glycolysis is the major energy supply pathway in postmortem muscle. PTMs can change the function and structure of pyruvate kinase, a rate-limiting enzyme in the glycolytic pathway, which can in turn affect meat quality. Beginning with an overview of the structure and function of pyruvate kinase, this article reviews the recent research progress on the effects of PTMs of pyruvate kinase on its function and structure and the effects of pyruvate kinase phosphorylation, acetylation and S-nitrosylation on meat quality.

OBJECTIVE: To explore the role of Compound 3k in osteoarthritis caused by glycolytic overactivity based on the hypoxia-inducible factor 1 alpha (HIF-1α)/ reactive oxygen species (ROS) pathway. METHODS: ATDC5 chondroblasts at logarithmic growth phase were taken to induce osteoarthritis in an in vitro cellular model by the action of 10 ng/mL interleukin-1β for 24 hours. The cytotoxicity of Compound 3k at different concentrations (0.25, 0.5, 1, 2.5, 5, 10, 15 μmol/L) was detected by cell counting kit8 assay, and the appropriate concentrations were selected for the subsequent experiments. The chondrocytes were randomly divided into control, model and treatment groups. The model group was induced with 10 ng/mL interleukin 1β, and the treatment group was pre-stimulated with Compound 3k for 2 hours and then co-cultured with interleukin 1β. The proliferation of the cells in each group was detected by the cell counting kit-8 assay; the inflammatory level of the cells in each group was detected by the ELISA kit; the ROS, extracellular lactate and glucose contents were detected using the kit; qRT-PCR and western blot were used to detect the levels of related inflammatory factors, interleukin-6 and tumor necrosis factor-α, glycolysis-related genes glucose transporter protein-1, glyceraldehyde 3-phosphate dehydrogenase, monocarboxylate transporter protein-1 and HIF-1α. RESULTS AND CONCLUSION: Compared with the control group, the model group showed a decrease in cell proliferative activity, active glycolysis level, manifested by an increase in extracellular lactate content (P < 0.001) and a decrease in glucose content (P < 0.001), interleukin-6 (P < 0.000 1) and tumor necrosis factor-α (P < 0.001). The expression levels of glycolysis-related genes glucose transporter protein-1 (P < 0.001), glyceraldehyde 3-phosphate dehydrogenase (P < 0.001), monocarboxylic acid transporter protein-1 (P < 0.001) and HIF-1α (P < 0.001) in the model group were all up-regulated, accompanied by oxidative stress and overproduction of ROS. Compared with the model group, Compound 3k treatment effectively increased cell proliferation activity and inhibited the level of overactive glycolysis (P < 0.001), while suppressing the expression of genes related to inflammation (P < 0.001) and glycolysis in osteoarthritic chondrocytes, inhibiting oxidative stress, downregulating the expression level of HIF-1α (P < 0.000 1) and decreasing the content of ROS. To conclude, Compound 3k inhibits interleukin-1β induced chondrocyte inflammation, and its mechanism may be related to glycolysis and HIF-1α/ROS mediated oxidative stress. [ABSTRACT FROM AUTHOR]

Pulmonary fibrosis is caused by repeated damage to the pulmonary alveolar epithelium, leading to abnormal epithelial-mesenchymal transition and myofibroblast production, resulting in the accumulation of extra cellular matrix and remodeling of the interstitium. Analogous to many tumor cells, pulmonary fibrosis involves metabolic reprogramming, encompassing alterations in carbohydrate, lipid, and amino acid metabolism. Notably, this reprogramming is marked by enhanced glycolysis, diminished fatty acid oxidation paired with augmented synthesis, and increased degradation of glutamine. Glycolysis efficiently and rapidly fulfills the energy requirements for the proliferation of macrophages and fibroblasts during fibrotic development. Additionally, the reprogramming of amino acid metabolism in activated fibroblasts not only facilitates collagen synthesis but also intensifies myofibroblast activation by generating reactive oxygen species (ROS) during the production of hydroxyproline.

Objective To explore the effects and mechanisms involved in glioma conditioned medium for inducing glycolysis and oncogenic mediators in macrophages. Methods Bone marrow derived macrophage (BMDM) induced by hypoxia and mouse glioma cell line GL261 conditioned medium (GCM)(GCM-BMDM) were used as a model. The mRNA level of M1 and M2 oncogenic mediators, hypoxia-inducible factor-1α (HIF-1α) and glycolysis associated genes in GCM-BMDM were detected by qPCR. The extracellular acidification rate (ECAR) of GCM-BMDM was detected by Seahorse bioenergy assay method. The protein levels of signal transducer and activator of transcription 6 (STAT6), signal transducer and activator of transcription 3(STAT3) and their phosphorylated forms p-STAT6 and p-STAT3 were examined by Western blot. Results GCM stimulated mRNA expression of Hif-1α and a variety of M1 and M2 oncogenic mediators in BMDM (P＜0.01). GCM upregulated the mRNA expression of multiple glycolysis associated genes (P＜0.01) and increased glycolysis level in BMDM (P＜0.001). The glycolysis level was reduced by incubation with lactate dehydrogenase inhibitor stiripentol (STP) (P＜0.05). STP down-regulated mRNA levels of Hif-1α and oncogenic mediators Il-1β, Il-6, Ido and Cd163 in GCM-BMDM(P＜0.01). STP decreased the ratio of p-STAT3 /STAT3 and p-STAT6 /STAT6 in GCM-BMDM (P＜0.05). Conclusions GCM increases glycolysis level and induces the pro-tumoral phenotypes in GAMs through promoting transcriptional regulation mediated by HIF-1α, STAT3 and STAT6. STP can effectively reduce glycolysis and transcriptional expression of oncogenic mediators in GAMs.

Objective: To analyze and explore the expression of TRIM29 in osteosarcoma and its potential molecular mechanism. E3 ubiquitination ligase TRIM29 is closely related to the malignant growth of tumors. Methods: The expression of TRIM29 gene in osteosarcoma was analyzed by Western blot, IHC and qRT-PCR, CCK8 and EDU were used to detect the value-added level of osteosarcoma cells after downregulation of TRIM29. Further, glucose uptake, lactate production and G6P were used to detect the changes of glycolysis level and analyze the underlying mechanism. A subcutaneous tumor model of BACB/C nude mice was established to observe the effect of downregulation of TRIM29 on the growth of transplanted tumors. Results: qRT-PCR results confirmed that the mRNA expression level of TRIM29 in osteosarcoma tissues was significantly higher than that in normal tissues. Similarly, Western blot and IHC results also confirmed that the protein level of TRIM29 in osteosarcoma tissues was significantly higher. After downregulating the expression of TRIM29 in osteosarcoma cells, CCK-8 and EDU experiments both showed that its value-added ability was weakened, on the contrary, its apoptosis rate was increased. In the G1 phase of cells, its lactate production, glucose consumption, G6P were also correspondingly weakened, and the glycolytic joint rate limiting enzymes HKII, PFKFB3, PKM, LDHAA, GLUT1 and other proteins were also correspondingly reduced. Similarly, in vivo experiments also showed that after downregulating the expression of TRIM29, the weight and growth rate were reduced accordingly. Conclusion: TRIM29 is highly expressed in osteosarcoma cells. After inhibiting the expression of TRIM29 in osteosarcoma cells, its cell proliferation ability and glycolysis level are decreased. TRIM29 inhibits the growth of osteosarcoma cells by restraining the glycolysis level of cells [ABSTRACT FROM AUTHOR]

Objective To investigate the effect of far upstream element binding protein 3 (FUBP3) mediated glycolysis on the differentiation and function of osteoblasts. Methods RT-qPCR was used to detect FUBP3 mRNA expression in peripheral blood of patients with brittleness fracture at 24 h after admission, and 1, 2, 3, and 4 w after treatment. RT-qPCR and Western blotting were used to detect FUBP3 mRNA and protein expression in the bone tissue of patients with fragility fracture. MC3T3-E1 cells were divided into sh-NC group, sh-FUBP3 group, pcDNA group, and PCDNA-FUBP3 group. The cell proliferation activity was detected with MTT and EdU. Western blotting was used to detect Runt-related transcription factor 2 (Runx2), osteopontin (OPN), glucose transporter 1(Glut1), and Glut3 proteins. Alkaline phosphatase (ALP) activity, glucose consumption, and lactic acid production were measured. Results The expression level of FUBP3 mRNA in peripheral blood of patients with fragility fracture was higher than that of patients with non-fragility fracture, and the expression levels of FUBP3 mRNA and protein in the bone tissue of patients with fragility fracture were higher than those in patients with non-fragility fracture (P<0.05). In peripheral blood of fragility fracture patients at 24 h after admission and 1, 2, 3 and 4 w after treatment, FUBP3 mRNA was found to decrease gradually with the increase of treatment time in a time-dependent manner. The expression level was the lowest at 4 w after treatment (P<0.05). Compared to those in sh-NC group, the mRNA and protein expressions of FUBP3 in sh-FUBP3 group decreased significantly. The cell activity, EdU positive cell ratio, glucose consumption, lactic acid production, and ALP activity increased significantly. The protein expressions of Glut1, Glut3, Runx2 and OPN were up-regulated (P<0.05). Compared to those in pcDNA group, the expressions of FUBP3 mRNA and protein in PCDNA-FUBP3 group increased significantly, while the cell activity, EdU positive cell ratio, glucose consumption, lactic acid production and ALP activity decreased significantly. The protein expressions of Glut1, Glut3, Runx2 and OPN were down-regulated (P<0.05). Conclusion FUBP3 expression is up-regulated in peripheral blood and bone tissue of patients with osteoporotic fractures. Knockdown of FUBP3 inhibits osteoblast proliferation, osteogenic differentiation, and glycolysis. Overexpression of FUBP3 inhibits the opposite. [ABSTRACT FROM AUTHOR]

Objective To investigate the effect of Hedyotis diffusa extract(HDE)on the proliferation of liver cancer cells and its relationship with sugar metabolism reprogramming and oxidative phosphorylation and analyze its possible mechanisms. Methods CCK-8 and EDU experiments were used to determine the effect of different concentrations(20,40,80 mg/mL)of HDE on the growth of liver cancer cell line SNU-368. Lactate dehydrogenase activity, glucose uptake, lactate production, extracellular pH, mitochondrial respiratory chain complex activity, and cellular oxygen consumption were measured to analyze the effect of HDE on aerobic glycolysis and oxidative phosphorylation in liver cancer cells. qRT-PCR experiments were used to detect the mRNA expressions of GLUT1, GLUT4, HK2, GPI, PFKL, ALDOA and HIF-1α in SNU-368 cells of different groups. Western blotting experiments were used to detect the protein expression of HIF-1α. A stable cell line overexpressing HIF-1α was constructed by lentivirus transfection of liver cancer cells SNU-368 and then intervened with HDE; the expression of HIF-1α mRNA and protein was detected with qRT-PCR and Western blotting. Results CCK-8 results showed that the HDE exhibited a concentration-dependent inhibitory effect on the proliferation of liver cancer cells(all P<0.05). Results from glucose metabolism-related tests indicated that the HDE could inhibit glucose uptake and lactate production, decrease lactate dehydrogenase activity, increase extracellular pH value, enhance cellular oxygen consumption, and elevate activities of mitochondrial respiratory chain complexes Ⅰ, Ⅱ, Ⅲ and Ⅳ(all P<0.05). qRT-PCR results revealed that the HDE suppressed the mRNA expressions of GLUT1, HK2, GPI, and ALDOA(all P<0.05). qRT-PCR and Western blotting experiments showed that compared to the control group, the expression of HIF-1α mRNA and protein in the HDE group was significantly reduced. However, when HIF-1α was overexpressed and HDE was added in the HIF-1α-LV group, the expression of HIF-1α mRNA and protein increased again compared to the HDE group. Conclusion HDE inhibits glycolysis and promotes oxidative phosphorylation to inhibit the proliferation of liver cancer cells, and its mechanism of action may be related to the inhibition of HIF-1α expression. [ABSTRACT FROM AUTHOR]

Copyright of Traditional Chinese Drug Research & Clinical Pharmacology is the property of Traditional Chinese Drug Research & Clinical Pharmacology Editorial Office and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Journal of Food Safety & Quality is the property of Journal of Food Safety & Quality Editorial Department and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Objective To investigate the expression of Thymosinβ10 (TMSB10) in gastric cancer and its molecular mechanism in promoting the progression of gastric cancer. Methods We collected pathological sections of 70 patients with gastric cancer in our hospital, detected expression of TMSB10 in gastric adenocarcinoma by immunohistochemistry, and analyzed its prognostic effect. In order to study the mechanism of action, the effects of TMSB10 on the proliferation and glycolysis of gastric cancer cells and its related mechanism were observed by transfection technique, CCK8 test, EDU assay, Transwell assay, scratch test, glycolysis assay and Western blot. Results Immunohistochemistry showed that TMSB10 was highly expressed in gastric cancer, while the expression level of TMSB10 was correlated with tumor size (P = 0.032, TNM stage (P = 0.002) and distant metastasis. In the mechanism study, we found that overexpression of TMSB10 promoted the proliferation, invasion, migration and glycolytic phenotype of gastric cancer cells through in vitro CCK-8 test, EDU assay, Transwel assay and glycolysis assay, and vice versa. Western blot results showed that overexpression of TMSB10 may regulate the occurrence of gastric cancer through up-regulation of the AMPK/mTOR signaling pathway. Conclusions TMSB10 promotes the proliferation, invasion, migration and glycolysis gastric cancer through the AMPK/mTOR signaling pathway. [ABSTRACT FROM AUTHOR]

AIM: To investigate the effects of sodium hydrosulfide (NaHS) on hexokinase 2 (HK2)-nucleo-tide-binding oligomerization domain-like receptor protein 3 (NLRP3)-gasdermin D (GSDMD) pathway and pyroptosis induced by lung ischemia/reperfusion (I/R) in rats. METHODS: Male Sprague-Dawley rats were divided into 6 groups: control group, control+NaHS group, I/R group, low-dose NaHS+I/R (L+I/R) group, medium-dose NaHS+I/R (M+I/R) group, and high-dose NaHS+I/R (H+I/R) group, with 6 rats in each group. The NaHS was administered via intraperitoneal injection at 1.5 mL, 30 min before modeling. The left lung tissues were collected 30 min after ischemia and 1 h after reperfusion, and the wet/dry weight ratio and total lung water content were recorded. Hematoxylin-eosin (HE) staining was used to examine lung tissue morphological changes. The levels of malondialdehyde (MDA), myeloper oxidase (MPO) and lactate in lung tissues were measured with test kits. ELISA was employed to determine the levels of interleukin-1p (IL-1p) and IL-18. The expression of glycolysis- and pyroptosis-related indicators was analyzed by Western blot, qRT-PCR and immunofluorescence staining. RESULTS: Compared with control group, the rats in NaHS group showed no significant differences in all laboratory tests (P>0. 05). The rats in I/R group exhibited significant lung injury, oxidative stress, increased lactate level, and up-regulated glycolysis and pyroptosis (P<0. 05 or P<0. 01). Compared with I/R group, the indicators in L+I/R group showed a downward trend (P<0. 01) or no difference (P>0. 05), while those in M+I/R group displayed a significant reduction (P<0. 05 or P<0. 01). However, the indexes in H+I/R group exhibited no significant differences in these tests (all P>0. 05). CONCLUSION: A moderate dose (56 xmol"L-1-kg-1) of NaHS mitigated the occurrence of pyroptosis by inhibiting the HK2-NLRP3-GSDMD pathway, thus contributing to the attenuation of lung I/R injury in rats. [ABSTRACT FROM AUTHOR]

Pulmonary fibrosis is caused by repeated damage to the pulmonary alveolar epithelium, leading to abnormal epithelial-mesenchymal transition and myofibroblast production, resulting in the accumulation of extra cellular matrix and remodeling of the interstitium. Analogous to many tumor cells, pulmonary fibrosis involves metabolic reprogramming, encompassing alterations in carbohydrate, lipid, and amino acid metabolism. Notably, this reprogramming is marked by enhanced glycolysis, diminished fatty acid oxidation paired with augmented synthesis, and increased degradation of glutamine. Glycolysis efficiently and rapidly fulfills the energy requirements for the proliferation of macrophages and fibroblasts during fibrotic development. Additionally, the reprogramming of amino acid metabolism in activated fibroblasts not only facilitates collagen synthesis but also intensifies myofibroblast activation by generating reactive oxygen species (ROS) during the production of hydroxyproline. [ABSTRACT FROM AUTHOR]

Copyright of Chinese Journal of Cancer Biotherapy is the property of Editorial Office of Chinese Journal of Cancer Biotherapy and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Objective To explore the effects and mechanisms involved in glioma conditioned medium for inducing glycolysis and oncogenic mediators in macrophages. Methods Bone marrow derived macrophage (BMDM) induced by hypoxia and mouse glioma cell line GL261 conditioned medium (GCM)(GCM-BMDM) were used as a model. The mRNA level of M1 and M2 oncogenic mediators, hypoxia-inducible factor-1α (HIF-1α) and glycolysis associated genes in GCM-BMDM were detected by qPCR. The extracellular acidification rate (ECAR) of GCM-BMDM was detected by Seahorse bioenergy assay method. The protein levels of signal transducer and activator of transcription 6 (STAT6), signal transducer and activator of transcription 3(STAT3) and their phosphorylated forms p-STAT6 and p-STAT3 were examined by Western blot. Results GCM stimulated mRNA expression of Hif-1α and a variety of M1 and M2 oncogenic mediators in BMDM (P＜0.01). GCM upregulated the mRNA expression of multiple glycolysis associated genes (P＜0.01) and increased glycolysis level in BMDM (P＜0.001). The glycolysis level was reduced by incubation with lactate dehydrogenase inhibitor stiripentol (STP) (P＜0.05). STP down-regulated mRNA levels of Hif-1α and oncogenic mediators Il-1β, Il-6, Ido and Cd163 in GCM-BMDM(P＜0.01). STP decreased the ratio of p-STAT3 /STAT3 and p-STAT6 /STAT6 in GCM-BMDM (P＜0.05). Conclusions GCM increases glycolysis level and induces the pro-tumoral phenotypes in GAMs through promoting transcriptional regulation mediated by HIF-1α, STAT3 and STAT6. STP can effectively reduce glycolysis and transcriptional expression of oncogenic mediators in GAMs. [ABSTRACT FROM AUTHOR]

Objective: To discuss the effects of different doses of ganoderic acid A (GAA) on the biological activities, glycolysis, and the expression of rate-limiting enzymes of non-small cell lung cancer (NSCLC) PC9 cells, and to clarify the mechanism. Methods: The NSCLC PC9 cells were cultured in vitro and divided into blank control group, low dose (25 µmol·L-1) of GAA group, medium dose (50 µmol·L-1) of GAA group, and high dose (100 µmol·L-1) of GAA group. The methylthiazolydiphenyltetrazolium (MTT) assay was used to detect the survival rates of the PC9 cells in various groups; Transwell chamber assay was used to detect the number of migration cells of the PC9 cells in various groups; the glucose uptakes of the PC9 cells in various groups were detected by glucose assay kit; the levels of ATP in the PC9 cells in various groups were detected by ATP assay kit; the levels of lactic acid in the PC9 cells in various groups were detected by lactate assay kit; the expression levels of hexokinase 2 (HK2) and pyruvate kinase M2 (PKM2) mRNA in the PC9 cells in various groups were detected by real-time fluorescence quantitative PCR (RT-qPCR) method; the expression levels of HK2 and PKM2 proteins in the PC9 cells in various groups were detected by Western blotting method. Results: The MTT assay results showed that, at 24, 48, and 72 h of culture, compared with blank control group, the survival rates of the cells in medium and high doses of GAA groups were significantly decreased (P<0. 05). At 72 h of culture, compared with low dose of GAA group, the survival rate of the cells in high dose of GAA group was significantly decreased (P<0. 05). The Transwell chamber assay results showed that compared with blank control group, the numbers of migration cells in medium and high doses of GAA groups were significantly decreased (P<0. 05); compared with low doses of GAA group, the number of migration cells in high dose of GAA group was significantly decreased (P<0. 05). Compared with blank control group, the glucose uptakes and levels of lactic acid in the cells in medium and high dose of GAA groups were significantly decreased (P<0. 05), and the level of ATP in the cells in high dose of GAA group was significantly decreased (P<0. 05). The RT-qPCR results showed that compared with blank control group, the expression levels of HK2 and PKM2 mRNA in the cells in medium and high doses of GAA groups were significantly decreased (P<0. 05). The Western blotting results showed that compared with blank control group, the expression levels of HK2 and PKM2 proteins in the cells in medium and high doses of GAA groups were significantly decreased (P<0. 05). Conclusion: Medium and high doses of GAA can inhibit the biological activities of proliferation and migration of the PC9 cells, reduce the glycolysis, and its mechanism may be related to the inhibition of the expressions of the key rate-limiting enzymes HK2 and PKM2. [ABSTRACT FROM AUTHOR]

Copyright of Practical Oncology Journal is the property of Journal of Practical Oncology Editorial Office and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

This study aimed to investigate the effects of nitric oxide (NO)-mediated hypoxia-inducible factor-1α (HIF-1α) on the glycolysis and tenderness of postmortem yak muscle and its regulatory mechanism. In this study, Yak Longissimus dorsi was injected with 0.9% saline (control), 200 μmol/L S-nitrosoglutathione (GSNO), 200 μmol/L GSNO + 100 μmol/L YC-1 (HIF-1α inhibitor) or 200 μmol/L GSNO + 50 μmol/L PD98059 and aged, and NO level, HIF-1α, mitogen-activated protein kinase/extracellular signal-regulated kinase (MAPK/ERK) pathway activation, glycolysis-related enzyme activities, and shear force of muscle were analyzed at different aging time points (3, 6, 9, 12, 24 and 72 h). The results revealed that NO levels in the GSNO group were significantly higher than those in the control group during 3–72 h (P < 0.05), reaching a peak at 6 h. ERK1/2 and p-ERK1/2 expression levels were higher in the GSNO group than the control and GSNO + PD98059 groups during 3–72 h (P < 0.05), reaching a peak at 24 h. HIF-1α expression level in the GSNO group was significantly higher than that in the control and GSNO + YC-1 groups (P < 0.05), peaking at 12 h. Hexokinase (HK), pyruvate kinase (PK) and lactate dehydrogenase (LDH) in the GSNO group reached their maximum values at 9, 12 and 12 h, respectively (P < 0.05) and were significantly higher than those in the control group; at 3, 12 and 72 h, the glycolytic potential in the GSNO group was significantly higher than that in the two other groups (P < 0.05); at 6, 9 and 72 h, the pH in the GSNO group was significantly lower than that in the other groups (P < 0.05). In addition, shear force and hematoxylin and eosin (HE) staining were used to assess the tenderness of yak meat. Shear force, myofiber cross-sectional area and diameter were lower and the space between myofibers was higher in the GSNO group than in the two other groups. In conclusion, during the early period of postmortem aging, NO mediates the MAPK/ERK signaling pathway, thereby activating HIF-1α expression and upregulating HK, PK and LDH activity, accelerating the rate of glycolysis of and reducing pH, and ultimately improving the tenderness of yak meat. The results of this study may serve as a potential regulatory mechanism for regulating the tenderness of yak meat and provide a theoretical basis for improving the theoretical system of glycolysis and tenderness during postmortem aging.

In order to clarify the relationship between the degree of glycolysis and water-holding capacity during the maturation of Tan sheep meat, the M. longissimus dorsi of six-month-old Tan sheep was aged at 4 ℃ postmortem and evaluated for drip loss, purge loss, calpain-1 activity, myofibril fragmentation index (MFI), ATP content, glucose content, glycogen content, lactic acid content, lactate dehydrogenase (LDH) activity, pyruvate kinase (PK) activity and pH after 0, 1, 2, 3, 4 and 8 days. The results showed that as maturation time increased, drip loss, purge loss and centrifugal loss increased first and then decreased (P < 0.05), reaching their maximum values on day 4. ATP and glycogen contents continued to decrease (P < 0.05). The contents of glucose and lactic acid increased first and then decreased (P < 0.05), and so did LDH activity (P < 0.05), reaching its maximum level on day 4. PK activity showed a constant decreasing trend (P < 0.05). The correlation analysis showed that glycogen content was negatively correlated with drip loss (P < 0.05) as well as purge loss and centrifugal loss (P < 0.01), and positively correlated with nuclear magnetic resonance (NMR) transverse relaxation times (T21, T22 and T23) (P < 0.05 or P < 0.01). LA content was significantly positively correlated with drip loss (P < 0.001) as well as purge loss and centrifugal loss (P < 0.01), but had no correlation with T21, T22 or T23. Therefore, the glycolysis process of Tan sheep meat was activated rapidly after slaughter, which caused change in the activity of glycolysis-related enzymes and the contents of metabolites, thereby resulting in changes in the water adsorption capacity of muscle proteins, and ultimately affecting the water-holding capacity of Tan sheep meat after slaughter.

Gastric cancer has extensive metastasis and high mortality, and its pathogenesis has not been fully understood. The advent of metabolomics has further brought metabolic regulation and cancer research into the spotlight. This article provides an overview of the important metabolic changes caused by gastric cancer, and their therapeutic significance is considered and prospected.

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AIM: To investigate the effects of cannabinoid receptor agonist WIN55212-2 (WIN) on acute lung injury (ALI) in septic mice, and to explore its potential mechanisms through glycolysis. METHODS: A mouse model of septic ALI was established by intraperitoneal injections of lipopolysaccharide (LPS). Male C57BL/6J mice were randomly divided into 4 groups (n=6) : (1) control group; (2) LPS group, receiving intraperitoneal injections of LPS at 10 mg/kg; (3) LPS+WIN group, receiving 1 mg/kg WIN intraperitoneally 30 min prior to LPS injection; (4) LPS+WIN+MHY1485 [mammalian target of rapamycin (mTOR) activator] group, receiving 10 mg/kg MHY1485 intraperitoneally 1 d before LPS injection and 1 mg/kg WIN plus 10 mg/kg MHY1485 30 min before LPS injection. Tissues were collected 24 h after modeling for analysis. Lung indexes were calculated, and histopathological changes of lung tissues were observed via hematoxylin-eosin (HE) staining. Inflammatory cytokines interleukin-1β (IL-1β) and IL-10 in lung tissues, and lactic acid and lactate dehydrogenase A (LDHA) in serum were quantified using ELISA. The levels of mTOR/hypoxia-inducible factor-1α (HIF-1α)/6-phosphofructo-2-kinase/fructose-2, 6-biphosphatase 3 (PFKFB3) signaling pathway-related proteins were assessed by Western blot. RESULTS: Compared with control group, the LPS group exhibited an increased lung index, significant lung tissue damage, an increase in IL-1β levels (P<0. 05), a decrease in IL-10 levels (P<0. 05), and elevated expressions of lactate and LDHA (P<0. 05), along with increased levels of phosphorylated mTOR (p-mTOR), HIF-1α and PFKFB3 proteins (P<0. 05). The LPS+WIN group showed improvements with a reduced lung index (P< 0. 05), lessened lung injury, decreased IL-1β levels (P<0. 05), increased IL-10 levels (P<0. 05), and lower levels of lactic acid, LDHA, p-mTOR, HIF-1α, and PFKFB3 (P<0. 05). Conversely, the LPS+WIN+MHY1485 group displayed increased lung indexes and lung tissue damage, elevated IL-1β levels (P<0. 05), reduced IL-10 levels (P<0. 05), and higher expressions of lactic acid, LDHA, p-mTOR, HIF-1α and PFKFB3 (P<0. 05) compared to the LPS+WIN group. CONCLUSION: WIN55212-2 mitigates sepsis-induced ALI, potentially by modulating the mTOR/HIF-1α/PFKFB3 signaling pathway, thereby inhibiting glycolysis and alleviating inflammatory responses. [ABSTRACT FROM AUTHOR]

Copyright of Practical Oncology Journal is the property of Journal of Practical Oncology Editorial Office and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Objective To investigate the changes and effects of glycolysis in Gefitinib resistance in non ‐ small cell lung cancer (NSCLC) . Methods NSCLC parental cells PC‐9 and A549 were cultured in vitro, and NSCLC Gefitinib‐resistant cells PC‐9‐GR and A549‐GR were constructed by the increasing concentration method. Cell resistance was identified by CCK‐8 and colony formation assay. The glucose metabolism and lactate production levels were detected using glucose and lactate assay kits, respectively. qRT ‐PCR and Western blot were used to detect the mRNA and protein levels of the key enzymes in glycolysis. After inhibition of glycolysis by 2‐deoxy‐ D‐glucose, the viability of cells and the changes of drug resistance to Gefitinib were observed. Results Compared with parental cells, the resistance of PC‐9‐GR and A549‐GR cells to Gefitinib was enhanced (all P<0.01), and glucose metabolism rate and lactate production level were increased (all P<0.01). The mRNA expression levels of HK2, LDHA and PFK and the protein levels of HK2, LDHA, PFKP and PKM2 were increased (all P<0.001). The inhibitory effect of 2‐DG on the activities of drug‐resistant cells was more significant than on those of their respective parental cells (all P<0.05), and to some extent, it could enhance the killing effect of Gefitinib on drug‐resistant cells. Conclusions Gefitinib resistance in NSCLC is accompanied by the activation of glycolysis, and is associated with increased expression of key enzymes in glycolysis. Inhibiting the levels or activities of glycolysis may be an effective measure to reverse the drug resistance of Gefitinib. [ABSTRACT FROM AUTHOR]

To investigate the effects and mechanism of anlotinib intervention on glycolysis, proliferation, colony formation and migration of human lung cancer NCI-H226 cells, to provide reference for in vitro test of lung cancer. Human lung cancer NCI-H226 cells were divided into control group which is without intervention, experimental group involving 10, 20, 40 μmol/L anlotinib, and positive control group involving 20 μg/mL cisplatin. The cell counting kit-8 (CCK-8), 5-acetylene-2' deoxyuracil riboside (EdU) staining, plate clone formation, lactic acid detection kit, glucose detection kit, Transwell assay, RT-qPCR and Western blotting (WB) assays were used to detect proliferation viability, proliferation, colony-formation ability, lactic acid content, glucose consumption level, cell migration number and expression level of related factor levels. The proliferation activity, proliferation rate, clone formation rate, lactate content, glucose consumption level, N-cadherin, vimentin and fibronectin (FN) of NCI-H226 cells in control group, experimental group and positive drug group. There were significant differences in mRNA and protein expression levels between groups (P<0.05). The cell proliferation activity of 20 and 40 μmol/L anlotinib and positive drug groups was higher than that of control group (P<0.05). The cell proliferation rate, clone formation rate, lactate content, glucose consumption level and mRNA and protein expression levels of N-cadherin, vimentin and FN in the experimental group and the positive drug group were higher than those in the control group (P<0.05). Anlotinib can significantly inhibit glycolysis, proliferation, colony formation and migration of human lung cancer NCI-H226 cells. [ABSTRACT FROM AUTHOR]

The aim of the experiment was to investigate the effects of different protein levels on the growth performance, serum biochemical indexes and meat quality of Tibetan sheep. Ninety 2- month-old male lambs of plateau type Tibetan sheep with similar initial body weight (15.40± 0.81) kg and good body condition were randomly divided into three groups with five replicates in each group and six lambs in each replicate. Each group was fed diets with protein levels of 12% (group a), 14% (group B) and 16% (group C). The whole experiment was divided into a pre-test period of 7 d and a formal period of 90 d. The results showed that: ① the differences in average daily weight gain, average daily feed intake and feed-to-weight ratio among the groups were not significant (P>0.05). ② The serum ghrelin activity of group A was higher than that of group B (P>0.05) and group C (P<0.05), the serum glucose content of group B was significantly lower than that of the other 2 groups (P<0.05), and the serum total protein content of group A was lower than that of group B (P<0.05) and group C (P>0.05). ③ Glycogen content of muscles in group C was significantly higher than group A (P<0.05). Malate dehydrogenase activity of muscles in group C was significantly higher than the other 2 groups (P<0.05). ④ Muscle fibre diameter was significantly higher in group C than in group B (P<0.05). Muscle fibre density was significantly higher in groups B and C than in group A (P<0.05). Cross sectional area was significantly higher in group B than in group C (P<0.05). In conclusion, a dietary protein level of 16% is favourable to enhance the growth performance of Tibetan sheep. At 14% protein level, it is beneficial to enhance the muscle quality of Tibetan sheep during the fattening period. [ABSTRACT FROM AUTHOR]

This study was performed in order to uncover the molecular mechanism by which postmortem glycolysis affects meat quality traits for the purpose of promoting the research and development of prediction technologies for the quality change of chilled Tan lamb and promoting the improvement of its processing, storage and transportation technologies. High-throughput sequencing technology was used for transcriptome sequencing and analysis of the hind leg meat from Yanchi Tan lambs after 0, 4 and 8 days of chilling. The results showed that the differential expression genes (DEGs) were mainly enriched in cellular amide metabolism, ATP metabolism, skeletal muscle contraction and ribosomes and involved in glycolysis, ribosomes and the p53 signaling pathway, and these DEGs constituted a key part of muscle cell function. The phosphofructokinase (PFKM), glyceraldehyde-3-phosphate dehydrogenase (GADPH), phosphoglycerate mutase 2 (PGAM2), enolase 3 (ENO3) and pyruvate kinase (PKM) genes were the core genes involved in the glycolytic metabolism of Tan lambs, which changed meat quality mainly by affecting the structure of muscle fibers, the degradation degree of structural proteins, the activity of glycolytic enzymes, the production of ATP and the activity of complexes.

Our purpose was to clarify the effect of CaCl2 treatment on the energy level and quality of Tan sheep meat during postmortem aging. Tan sheep hind leg meat was injected with 200 mmol/L CaCl2 solution, and aged at 4 ℃ for 0, 2, 4, 6, and 8 days. The protein expression of phosphofructokinase (PFKM) was detected by sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE) and Western blot to verify whether the glycolysis pathway could be activated by CaCl2. At the same time, the energy level and meat quality indexes were measured during postmortem aging to analyze the mechanism by which the glycolysis pathway affects the metabolic level and quality of Tan sheep meat. The results showed that the protein expression of PFKM decreased during postmortem aging, indicating activation of the glycolytic pathway. CaCl2 treatment accelerated the glycolysis process after slaughter, thereby promoting the decomposition of glycogen, increasing the production of lactic acid, and resulting in a rapid decrease in pH. Water-holding capacity (WHC), myofibril fragmentation index (MFI) and b* value were higher and shear force and a* were lower in the treatment group than in the control and blank groups. Therefore, CaCl2 could affect the color, WHC and tenderness of Tan sheep meat at different aging stages. By accelerating the decrease of pH and the accumulation of energy metabolites, the glycolytic pathway increased the level of energy metabolism during postmortem aging, while inhibiting the production of oxymyoglobin, activating the activity of calpain, changing the structure of myofibrils and shortening the space between muscle protein molecules, which accelerated the process of myofibril fragmentation and the hydrolysis of myofibrillar protein, and led to a deterioration in meat color and an increase in water loss and meat tenderness.

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Copyright of Journal of Henan Agricultural Sciences is the property of Editorial Board of Journal of Henan Agricultural Sciences and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

BACKGROUND: Glycolysis is essential for osteoclast differentiation and bone resorption of mature osteoclasts is mainly dependent on glycolysis. Pyruvic acid, as the end product of glycolysis, plays an important role in the metabolism of the three nutrients. OBJECTIVE: To observe the effect of pyruvic acid on osteoclast differentiation. METHODS: The toxicity of different concentrations of pyruvic acid (0.1, 1, 10, 20, 30, 50 mmol/L) to RAW264.7 cells was detected by cell counting kit-8 assay, and the safe concentration of pyruvic acid was selected. RAW264.7 cells were grouped into interventions: blank control group was cultured with a complete medium (α-MEM medium containing volume fraction 10% fetal bovine serum and 1% double antibodies); control group was cultured with a complete medium containing nuclear factor κB receptor activating factor ligand, and experimental group was cultured with a complete medium with nuclear factor κB receptor activating factor ligand and different concentrations of pyruvic acid, followed by tartrate-resistant acid phosphatase staining, cytoskeletal F-actin staining, RTqPCR assay, western blot assay and bone resorption lacuna assay. RESULTS AND CONCLUSION: (1) The maximum half inhibitory concentration of pyruvic acid on RAW264.7 cells was 8.923 mmol/L, and 0.1, 1, 5 mmol/L were selected as the safe concentrations for subsequent experiments. (2) Tartrate-resistant acid phosphatase staining revealed that 1 mmol/L pyruvic acid promoted the differentiation of RAW264.7 cells into osteoclasts. (3) F-actin staining showed that 1 mmol/L pyruvic acid promoted the formation of osteoclast F-actin ring, while 5 mmol/L pyruvic acid did not interfere with the formation of osteoclast F-actin ring. (4) RT-qPCR assay indicated that pyruvic acid within the safe concentration range had no significant effect on the relative mRNA expression of osteoclast differentiation related genes nuclear factor of activator T-cells and tartrate-resistant acid phosphatase. (5) Western blot assay showed that 0.1 and 1 mmol/L pyruvic acid within the safe concentration range had no significant effect on the protein expression of nuclear factor of activator T-cells, while 5 mmol/L pyruvic acid inhibited the protein expression of nuclear factor of activator T-cells, and 0.1, 1, and 5 mmol/L pyruvic acid promoted the expression of osteoclast differentiation related protein c-Fos. (6) 1 mmol/L pyruvic acid promoted the formation of bone resorption lacunae in osteoclasts. (7) To conclude, 1 mmol/L pyruvic acid can promote the differentiation of receptor activator for nuclear factor-κB induced RAW264.7 cells into osteoclasts in vitro. [ABSTRACT FROM AUTHOR]

AIM: Utilizing a murine model of nonalcoholic fatty liver disease （NAFLD）, we investigated alterations in hepatic protein expression of glucose metabolism enzymes during the progression from nonalcoholic fatty liver （NAFL） to nonalcoholic steatohepatitis （NASH）. METHODS: Male C57BL/6J mice were randomly divided into control diet （CD） group （n=24） and high-fat diet （HFD） group （n=24）. Six mice in each group were euthanized at 8, 12, 16 and 20 weeks. Changes in body weight, liver weight and serum biochemical parameters were monitored. Hepatic steatosis was evaluated by HE staining and oil red O staining. The NAFLD activity score（ NAS） was determined to identify the timepoint of NAFL to NASH transition. Western blot analysis was conducted to examine alterations in glucose metabolism enzyme expression. Correlations between the protein levels and NAS were analyzed to elucidate the associations with NAFLD progression. RESULTS: Compared with CD-fed mice, HFD-fed mice exhibited increased body weight starting at 4 weeks, markedly elevated liver weight at 16 weeks, increased serum alanine aminotransferase and glucose levels after 12 weeks, and increased serum total cholesterol level after 16 weeks （all P<0. 05）. Histological assessments including HE staining, oil red O staining and NAS determination signified that most HFD-fed mice developed NASH at 16 weeks. Compared with CD-fed mice, HFD-fed mice displayed up-regulated hepatic protein expression of glycolysis-related enzymes, hexokinase 1 （HK1）, HK2, pyruvate kinase M2 （PKM2） and lactate dehydrogenase A （LDHA）, at 16 weeks （all P<0. 05）, while gluconeogenesis-related enzymes, glucose-6-phosphatase catalytic subunit （G6PC）, fructose-1, 6-bisphosphatase 1（ FBP1） and phosphoenolpyruvate carboxykinase 1（ PCK1）, were decreased（ all P<0. 05）. Remarkably, HK2, PKM2, LDHA, G6PC, PCK1 and pyruvate carboxylase （PC） protein levels exhibited significant alterations between 8 and 20 weeks in HFD-fed mice （all P<0. 05） and displayed marked correlations with NAS, among which PKM2 and PC showed strong positive correlation, while PCK1 exhibited robust negative correlation. CONCLUSION: The protein expression levels of glucose metabolism enzymes G6PC, PCK1, PC, HK2, PKM2 and LDHA are notably altered during NAFL to NASH progression, implying that targeting these enzymes may aid in impeding NAFLD progression. [ABSTRACT FROM AUTHOR]

Copyright of Journal of East China University of Science & Technology is the property of Journal of East China University of Science & Technology Editorial Office and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

This study was conducted to investigate the regulatory mechanism of reactive oxygen species (ROS) on the glycolysis pathway of bovine muscle and its impact on meat tenderness at the early stage of postmortem cold storage. Fresh beef was treated with hydrogen peroxide (H2O2) as a major ROS, N-acetyl-L-cysteine (NAC) as an ROS scavenger, or physiological saline as a control before being stored at 4 ℃. After 0.5, 6, 12, 24, and 48 hours, the glycolysis level and tenderness indices were assessed. In addition, tandem mass tag (TMT)-labeled quantitative proteomics was used for protein identification and quantitative analysis of the samples after 24 hours and for screening of differential proteins in the glycolysis pathway. The findings showed that the glycolysis level increased significantly in the H2O2-treated group, and glycogenolysis and lactic acid accumulation were significantly higher than those in the other two groups (P < 0.05). In contrast, the glycolysis process was significantly suppressed by NAC treatment. The H2O2-treated group reached the ultimate pH after 12 hours, 12 and 36 hours earlier than the control and NAC groups, respectively. The shear force of the H2O2-treated group reached its maximum after 12 hours, and the myofibrillar fragmentation index (MFI) was significantly greater than that of the other two groups after 6–48 hours (P < 0.05), indicating that a higher ROS level can accelerate the tenderization of bovine muscle by enhancing the glycolysis capacity during postmortem refrigeration. Totally eight up-regulated proteins and two down-regulated proteins in the glycolysis pathway were identified in the H2O2-treated versus control groups after 24 hours of refrigeration. Among these proteins, the up-regulated core proteins of phosphoglycerate mutase (PGAM), enolase (ENO), and pyruvate dehydrogenase E1 subunit beta (PDHB) coordinated with the down-regulated pyruvate dehydrogenase E1 subunit alpha (PDHA) to accelerate the glycolysis process. In conclusion, ROS can speed up glycolysis and consequently improve meat tenderness by regulating the expression of key proteins in the glycolysis pathway.

Objective To study the expression of Xklp2 target protein (targeting protein for Xenopus kinesin-like protein2, TPX2) in pancreatic carcinoma and its potential value in predicting prognosis. Methods Based on 200 genes related to glycolysis, the information of pancreatic patients was obtained from TCGA and GEO databases, and the characteristics of glycolysis metabolism of the latter were evaluated. At the same time, the metabolic characteristics and differential genes of the patients were evaluated, the risk model was established by Cox regression and Lasso regression analysis, and the key glycolysis related gene TPX2 was obtained. The prognostic validity of the model was verified by GEO database based on the expression of prognostic genes, the overall survival (OS) of patients with pancreatic cancer, the difference in the expression of prognostic genes between normal pancreatic tissue and pancreatic cancer was analyzed and finally the function of prognostic genes was verified at the cellular level. Results The case cohort was divided into three characteristic groups: high, medium and low glycolysis metabolism. Patients with low-rate glycolysis metabolism had certain survival advantages. TPX2 was the key gene of this model. Pancreatic cancer patients showed high expression of TPX2 and had poor prognosis. Knocking down TPX2 at cellular level can inhibit the proliferation and colony formation of pancreatic cancer cells. Conclusions The model based on glycolysis metabolism can effectively predict the prognosis of patients with pancreatic cancer. TPX2 is expected to become a potential marker gene for predicting the prognosis of pancreatic cancer.

Copyright of Journal of Food Safety & Quality is the property of Journal of Food Safety & Quality Editorial Department and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Glucose metabolic reprogramming is an important pathophysiological alteration during tumor development. Recent studies have revealed that endometriosis (EMs) has similar reprogramming of glucose metabolism to tumor, namely the transition from mitochondrial oxidative phosphorylation to aerobic glycolysis. Glucose metabolic reprogramming, characterized by increased glucose uptake, increased lactic acid production, and decreased production of reactive oxygen species, is closely associated not only with disease progression of EMs, but also with decreased oocyte quality and impaired endometrial receptivity in patients. This review systematically reviews the research progress of glucose metabolic reprogramming in EMs, providing deeper insight into the pathophysiological mechanism of EMs [ABSTRACT FROM AUTHOR]

Macrophages are sentinels on the front line of tissue defense and an important weapon for the body to fight against invading pathogens. Their metabolic patterns and functions are closely related to the development and outcome of diseases. In general, macrophages preferentially select the oxidative phosphorylation of glucose （OXPHOS） pathway to metabolize energy production, and in hypoxic environments, glycolysis is the predominant. However, tumor macrophages can also produce energy through glycolysis in the presence of sufficient oxygen, which is the classic "Warburg effect". Studies have shown that the reprogramming of glucose metabolism in M1 type macrophages is similar to that of tumor cells, showing that aerobic glycolysis is dominant and OXPHOS is supplemented, while M2 type macrophages are just the opposite, so blocking glucose metabolism reprogramming can effectively inhibit inflammation reaction. This review focuses on the key role of macrophages in the regulation of inflammatory diseases and the possible mechanism of there programming of glucose metabolism, in order to provide new strategies for the prevention and treatment of immune and metabolic related diseases. [ABSTRACT FROM AUTHOR]

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Copyright of Chinese Journal of Cancer Biotherapy is the property of Editorial Office of Chinese Journal of Cancer Biotherapy and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Shipin Kexue/ Food Science is the property of Food Science Editorial Department and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Objective To observe the ameliorative efficacy of dihydromyricetin (DHM) on diabetic cardiomyopathy (DCM), and reveal its effect and underlying mechanism of improving myocardial glucose metabolism. Methods DCM model was established in C57BL/6J male mice by high-fat diet combined with intraperitoneal injection of streptozotocin (STZ). The mice were subsequently divided into control group (CON, normal diet), DCM group (high-fat diet), and DCM+DHM group (high-fat diet and DHM), with 15 animals in each group. After 13 weeks of intervention, echocardiography and glucose tolerance test were performed before sacrifiction. After execution, the myocardial morphology was observed with HE, Masson, and Sirius Red staining, and serum biochemical indexes were detected. The expression levels of genes and proteins related to glucose absorption and glycolysis in myocardial tissue were determined by immunofluorescence assay and qRT-PCR. The differentially expressed genes and their enriched signal pathways were analyzed with RNA-Seq technique. Results Both the cardiac systolic and diastolic functions were significantly impaired in the DCM group, accompanied with obvious inflammatory cell infiltration and increased levels of serum myocardial injury markers, such as CK, CK-MB and LDH (P < 0.01) when compared with the conditions in the CON group. Obvious myocardial fibrosis was observed in the myocardial tissue of DCM group, and elevated mRNA levels of fibrosis related molecules, TGF-β1, α-SMA and Timp (P < 0.05, P < 0.01), as well as abnormal glycolipid metabolism indexes, including glucose tolerance, blood glucose, TC, TG, LDL-C and HDL-C (P < 0.05, P < 0.01) were found. The levels of glucose absorption related genes GLUT1 and GLUT4, as well as glycolysis related genes HK1, HK2, PFK, LDH and PKM were all remarkably decreased in the myocardium (P < 0.05). However, DHM intervention greatly improved the impaired cardiac functions, ameliorated myocardial fibrosis and injury, and corrected abnormal glycolipid metabolism in the DCM mice. DHM also promoted the expression of the genes related to glucose absorption and glycolysis at mRNA and protein levels. The results of RNA-seq showed that the expression of several genes related to metabolic regulation was significantly changed after DHM intervention, among which NR4A1 might be a potential target of DHM. Conclusion DHM ameliorates the cardiac function of DCM mice, which may be closely associated with the improvement of glucose absorption and glycolysis of cardiomyocytes.

[Objectives] The present study aimed to explore the effects of fine particulate matters (PM2.5) from pig house on polarization-related metabolism including arginine metabolism and glycolysis and the TLR4-NF-κB signaling pathway in porcine alveolar macrophages. [Methods] The experiment used porcine alveolar macrophage cell line(3D4/21)as the cell model, and set different concentrations of PM2.5 (0, 25, 50 and 100 μg·mL-1) and different treatment time(4, 8, 12, 16, 20 and 24 h)for the cell treatment, and the cells were collected to measure arginine metabolism, glycolysis and related indicators of the TLR4-NF-κB signaling pathway. [Results]The results showed that after 12 hours of PM2.5 treatment, the concentration of nitric oxide (NO) in the cell supernatant gradually increased with the raising concentration of PM2.5. When the PM2.5 concentration was higher than 50 μg·mL-1, the NO concentration reached a significant level as compared with the control group (P<0.01). The cells were cultured for different time with 50 μg·mL-1 PM2.5, the results showed that the concentration of NO in cell supernatant gradually increased within 16 hours treatment, with the prolongation of the cell treatment time, the effect of PM2.5 on the cells gradually decreased. Further, the treatment of PM2.5 reduced the activity of arginase in the cells, and the 50 μg·mL-1 treatment of PM2.5 showed a significant difference(P<0.01). At the same time, with the raising concentration of PM2.5, the value of lactate production/glucose consumption (L/G) was increased (P<0.05), indicating that the ratio of intracellular glucose to lactate conversion increased, and the mRNA expression levels of glycolysis-related genes GLUT-1 and GAPDH significantly increased (P<0.05); 100 μg·mL-1 PM2.5 significantly increased the mRNA expression level of IL-1β (P<0.01); and after 50 μg·mL-1 PM2.5 treatment, the mRNA expression level of the M2 macrophage marker CD206 significantly decreased (P<0.05). The TLR4-NF-κB signaling pathway was significantly activated after PM2.5 treatment(P<0.05). [Conclusions]These results indicated that PM2.5 from pig house promoted the occurrence of inflammatory response in porcine alveolar macrophages, and at the same time promoted the metabolic conversion of intracellular arginine and glucose metabolism to M1 phenotypic characteristics. [ABSTRACT FROM AUTHOR]