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Cases of acute tonsillitis, a common disease in the emergency department, are mostly mild and those complicated by severe pneumonia and acute respiratory distress syndrome are rarely reported.

Objectives: The aim of this study was to establish a quantitative syndrome differentiation model with logistic regression analysis for phlegm and blood stasis syndrome (PBSS) in coronary heart disease (CHD) to offer methodology guidance for the quantitative syndrome differentiation of Traditional Chinese Medicine (TCM). Design: Tongue, face, and pulse information of each subject was obtained using the TCM-intelligent diagnosis instruments. Logistic regression model was used to construct the syndrome diagnosis model. The area under receiver operating characteristic curve (ROC-AUC) was used to evaluate the diagnostic value of the model. Subjects: Among the 141 subjects, 83 belonged to the PBSS group, and 58 belonged to the non-PBSS group. Results: The independent indexes used to predict PBSS in patients with CHD were length of the crack (LC) (p = 0.002), number of ecchymosis (NE) (p

Objective: The aim of our study is to investigate the relationship between podocyte autophagy and apoptosis induced by Puromycin Aminonucleoside (PAN) and to clarify its mechanism.Methods: Podocyte...

Lipoprotein-associated phospholipase A2 (Lp-PLA2) and high-sensitivity C-reactive protein (hs-CRP) have been reported to be associated with cardiovascular disease (CVD). However, whether the combination of these two markers can improve the prediction of CVD is unknown.A total of 1,921 participants without CVD, aged 40 years or older, were enrolled from 2010 to 2011. Plasma Lp-PLA2 and hs-CRP were measured at baseline. Participants were subsequently followed until December 2015. We identified a total of 148 cardiovascular events (myocardial infarction, stroke, and all-cause death). Cox proportional-hazard models were used to determine the association between two independent markers and cardiovascular outcomes. The C statistic, Net Reclassification Improvement (NRI), and Integrated Discrimination Improvement (IDI) were used to determine the utility of the two markers in predicting cardiovascular risk.After adjustment for potential confounders, compared with the first quartile, hazard ratios (HRs) with 95% confidence interval (CI) for the third and fourth quartiles for Lp-PLA2 were 2.09 (1.17-3.73) and 2.62 (1.48-4.67), respectively, and HRs with 95%CI for the fourth quartile for hs-CRP was 1.78 (1.08-4.67). Compared with conventional risk factors, the combination of hs-CRP and Lp-PLA2 provided greater incremental information, and the C statistic increased by 0.013. The NRI and IDI were also statistically significant for cardiovascular events (P = 0.004 and P < 0.001, respectively).Hs-CRP and Lp-PLA2 have complementary effects in predicting cardiovascular outcomes in adults aged 40 years or older.

As a prevalent tumor among women, breast cancer is still an incurable disease due to drug resistance. In this study, we report microRNA‐221 to have a significant effect on breast cancer resistance to adriamycin. The microRNA‐221 is elevated in tumor tissue compared with nearby nontumor samples, as well as in breast cancer cell line with adriamycin resistance (MCF‐7/ADR) compared to its parental line (MCF‐7) and the normal breast epithelial cell line (MCF‐10A). Enforced level of microRNA‐221 promotes cancer resistance to adriamycin, which in turn sustains cell survival and exacerbates malignant formation. Reciprocally, the silence of microRNA‐221 in cancer cells augments the sensitivity to chemotherapy, thereby resulting in enhanced apoptosis of MCF‐7/ADR cells. Mechanistically, we identify PTEN as a direct target of microRNA‐221, which was conversely associated with a microRNA‐221 level in breast tumors. The knock‐down of PTEN partially reversed the stimulatory role of microRNA‐221 in the modulation of the Akt/mTOR signaling. Taken together, these findings suggest microRNA‐221 suppresses PTEN transcription and activates Akt/mTOR pathway, which in turn enhances breast cancer resistance to adriamycin and promotes cancer development. Our data thus illuminate the microRNA‐221/PTEN axis may act as a promising strategy for the treatment of chemotherapy‐resistant breast tumors., The miR‐221 suppresses PTEN transcription and activates Akt/mTOR pathway, which in turn enhances breast cancer resistance to adriamycin and promotes cancer development.

The trichomonad species Tetratrichomonas buttreyi and Pentatrichomonas hominis have been reported in the bovine digestive tract in only a few studies, and the prevalence and pathogenicity of these two protists in cattle herds remain unknown. In this study, the prevalence of T. buttreyi and P. hominis in yellow cattle, dairy cattle, and water buffalo in Anhui Province, China, was determined with a PCR analysis of the small subunit ribosomal RNA genes. The overall infection rates for T. buttreyi and P. hominis were 8.1% and 5.4%, respectively. Double infections were found in 15 (1.6%) samples from four farms. The prevalence of P. hominis in cattle with abnormal feces was significantly higher than that in cattle with normal feces (χ2 = 13.0, p

OBJECTIVE To observe the expression of N-methyl-D-aspartate (NMDA), apoptosis and the effect on neurological function recovery in rat model with middle cerebral artery occlusion (MCAO). Diffusion kurtosis imaging (DKI) was used to evaluate crossed cerebellar diaschisis (CCD) and to provide experimental and theoretical basis for the clinical treatment. MATERIALS AND METHODS The MCAO models were established in rats. Eighty-four rats were randomly and evenly divided into 7 groups, including control group, 6-h group, 12-h group, 24-h group, 48-h group, 7-day group and 14-day group. The rats were scanned by MRI at the above time points. Then, rats were sacrificed for H&E staining, immunohistochemical staining and TUNEL staining to detect the expression of NMDA in the core infarct area and cerebellum. At the end, the discussion of relationships between molecular biology and MRI parameters (ADC derived from DWI, and MD, MK and FA derived from DKI) was performed. RESULTS The values of MD, ADC and FA in MCAO rats were all lower than those in the control group. All MRI parameters of the contralateral cerebellum were lower than those of the ipsilateral cerebellum (p

Background: The New Nurses who lack the ability to recognize and manage anaphylactic shock can endanger the patients. In this study, we explored the effect of a simulated scenario designed to improve nurses’ understanding of their roles and responsibilities during the rescue of a patient with anaphylactic shock.Methods: The program of a simulation-based training was designed to teach learners to recognize the signs and symptoms of anaphylactic shock, place the patient in the correct position, stop ongoing intravenous infusion of the antibiotic which trigger the anaphylactic shock, restart an intravenous infusion on a new infusion apparatus, give 100% oxygen via a nasal cannula or mask, preserve airway patency, call the rapid response team (RRT), and correctly administer the medications prescribed by the clinician. Instructors evaluated each learner’s skills and behaviors by using a clinical competency questionnaire. All learners then completed the Chinese version of the Simulation Design Scale (SDS) and participated in semi-structured interviews with their instructors after the training.Results: All learners showed significant improvements in the 6 competencies assessed by the clinical competency questionnaire after the simulation-based training (all PConclusions: The simulation-based training in anaphylactic shock is a potentially viable and effective method to teach new registered nurses to manage clinical incidents.

Purpose Clinical approach for staging cerebral venous sinus thrombosis (CVST) depends on the duration from symptom onset to clinical diagnosis, which is subjective and may be incorrect. To investigate if T1-weighted signal characteristics of the thrombus can be used for staging the thrombus on segment level and predicting endovascular therapy outcome. Methods Ninety-one CVST patients underwent non-contrast-enhanced T1-weighted 3D variable-flip-angle fast-spin-echo (T1-SPACE) and 29 of them received endovascular therapy. We divided the 91 patients into acute, subacute, and chronic CVST stage according to the clinical approach, and then analyzed the T1 weighted signal characteristics (i.e., thrombus shape and signal intensity) of the thrombus at each stage. To investigate the endovascular therapy outcome associated with the thrombus stage and signal characteristics, we evaluated the thrombolytic ratio on patient level and recanalization rate on segment level, respectively. Results The thrombi at acute or chronic stage were depicted as isointense signals but as hyperintense signals at subacute stage. Compared to the thrombus at acute stage, the thrombus at chronic stage was contractive and can be distinguished. Developing thrombi at transition periods of acute-to-subacute or subacute-to-chronic stage were found appearing mixed iso-/hyper-intense signals. On patient’s level, the patients at earlier stage had higher thrombolytic ratio (acute: 80.7 ± 18.3%, subacute: 62.6 ± 36.3%, chronic: 22.9 ± 24.2%). On segment level, the thromboembolic segments of isointense or mixed iso-/hyper-intense thrombi at non-chronic stage had good thrombolytic outcome. Conclusion T1-weighted signal characteristics of the thrombus can be used for staging CVST and predicting the endovascular therapy outcome.

We aimed to elucidate the differences in genomic methylation patterns between ADLI and non-ADLI patients to identify DNA methylation-based biomarkers. Genome-wide DNA methylation patterns were obtained using Infinium MethylationEPIC (EPIC) BeadChip array to analyze 14 peripheral blood samples (7 ADLI cases, 7 non-ADLI controls). Changes in the mRNA and DNA methylation in the target genes of another 120 peripheral blood samples (60 ADLI cases, 60 non-ADLI controls) were analyzed by real-time polymerase chain reaction and pyrosequencing, respectively. A total of 308 hypermethylated CpG sites and 498 hypomethylated CpG sites were identified. Significantly, hypermethylated CpG sites cg06961147 and cg24666046 in TANC1 associated with ADLI was identified by genome-wide DNA methylation profiling. The mRNA expression of TANC1 was lower in the cases compared to the controls. Pyrosequencing validated these two differentially methylated loci, which was consistent with the results from the EPIC BeadChip array. Receiver operating characteristic analysis indicated that the area under the curve of TANC1 (cg06961147, cg24666046, and their combinations) was 0.812, 0.842, and 0.857, respectively. These results indicate that patients with ADLI have different genomic methylation patterns than patients without ADLI. The hypermethylated differentially methylated site cg06961147 combined with cg24666046 in TANC1 provides evidence for the diagnosis of ADLI.

Background and Aims:Rabdosia japonica var. glaucocalyx is a traditional Chinese medicine (TCM) for various inflammatory diseases. This present work aimed to investigate the protective effects of R. japonica var. glaucocalyx glycoproteins on lipopolysaccharide (LPS)-induced acute lung injury (ALI) and the potential mechanism.Methods: Glycoproteins (XPS) were isolated from R. japonica var. glaucocalyx, and homogeneous glycoprotein (XPS5-1) was purified from XPS. ANA-1 cells were used to observe the effect of glycoproteins on the secretion of inflammatory mediators by enzyme-linked immunosorbent assay (ELISA). Flow cytometry assay, immunofluorescence assay, and Western blot analysis were performed to detect macrophage polarization in vitro. The ALI model was induced by LPS via intratracheal instillation, and XPS (20, 40, and 80 mg/kg) was administered intragastrically 2 h later. The mechanisms of XPS against ALI were investigated by Western blot, ELISA, and immunohistochemistry.Results:In vitro, XPS and XPS5-1 downregulated LPS-induced proinflammatory mediators production including tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), IL-6, and nitric oxide (NO) and upregulated LPS-induced IL-10 secretion. The LPS-stimulated macrophage polarization was also modulated from M1 to M2. In vivo, XPS maintained pulmonary histology with significantly reducing protein concentration and numbers of mononuclear cells in bronchoalveolar lavage fluid (BALF). The level of IL-10 in BALF was upregulated by XPS treatment. The level of cytokines including TNF-α, IL-1β, and IL-6 was downregulated. XPS also decreased infiltration of macrophages and polymorphonuclear leukocytes (PMNs) in lung. XPS suppressed the expression of key proteins in the TLR4/NF-κB signal pathway.Conclusion: XPS was demonstrated to be a potential agent for treating ALI. Our findings might provide evidence supporting the traditional application of R. japonica var. glaucocalyx in inflammation-linked diseases.

Background. The aim was to develop a diagnostic questionnaire for damp phlegm pattern and blood stasis pattern in coronary heart disease patients (CHD-DPBSPQ). Methods. The standard procedures of questionnaire development were carried out to develop and assess CHD-DPBSPQ. The patients were assessed using the CHD-DPBSPQ, CHD-DPPQ, and CHD-BSPQ. Four methods were used to select the items on the CHD-DPBSPQ in a pilot study based on data from a Guizhou tertiary grade A hospital. Cronbach’s alpha and the split-half reliability, test-retest reliability, content validity, criterion validity, construct validity, and convergent validity were determined in a validation study using a nationwide sample. Results. After item selection, the CHD-DPBSPQ contained 15 items in two domains: the phlegm domain (9 items) and the blood stasis domain (6 items). For the CHD-DPBSPQ, the alpha coefficient was 0.88, the split-half coefficient was 0.90, and the intraclass correlation coefficient was 0.83. The range of the item-level content validity index (I-CVI) was 0.71 to 1.0 and that of the scale-level content validity index/average (Scale-CVI/Ave) was 0.97. The domain scores on the CHD-DPBSPQ were in close relation to the scores on a questionnaire for damp phlegm pattern in coronary heart disease patients (CHD-DPPQ) and a questionnaire for blood stasis pattern in coronary heart disease patient (CHD-BSPQ) (P<0.01). The root mean square error of approximation (RMSEA) was equal to 0.05 (90% CI: 0.044, 0.059). Convergent validity was demonstrated with a moderate correlation. Conclusion. The CHD-DPBSPQ is a reliable and valid instrument.

The research aims to explore the roles and regulatory mechanisms of the circular RNA (circRNA) ZNF292 (circZNF292) in OGD-induced damage in H9c2 cells. The H9c2 cells were treated by OGD and/or transfected with circZNF292, si-circZNF292, pc-Bcl-2/adenovirus E1B-19 kDa-interacting protein 3 (BNIP3) or corresponding controls. Cell viability was detected with the CCK-8. The protein expression levels of the Bax, caspase-3, Beclin-1, p62, LC3, BNIP3, Wnt3a, β-catenin and mammalian target of rapamycin (mTOR) were individually determined via western blot. qRT-PCR was used to examine the circZNF292 expression level. The apoptotic rate was determined by the Annexin V-FITC/PI with flow cytometer. The production of the circZNF292 was promoted by OGD. Abundant circZNF292 released OGD-induced damage by up-regulating cell viability and Wnt3a/β-catenin or mTOR proteins, but down-regulating apoptosis and autophagy. circZNF292 had an opposite effect on these elements mentioned above. Besides, BNIP3 was negatively adjusted by the circZNF292. The BNIP3 overproduction destroyed the protective effect of circZNF292 on H9c2. circZNF292 released OGD-induced damage in the H9c2 cells by targeting the BNIP3 through Wnt/β-catenin and mTOR activation.

Background: Myocardial ischemia is the main reason for ischemic heart disease. Baicalin is a plant-derived flavonoid with cardio-protective activity. Herein, we tested the influences of baicalin on cardiomyocytes H9c2 apoptosis aroused by hypoxia stimulation. Methods: Firstly, H9c2 cells were subjected to hypoxia and/or baicalin exposure. Cell viability and apoptosis, along with hypoxia-inducible factor 1α (HIF1α) and Bcl-2/adenovirus E1B 19-KDa interacting protein 3 (BNIP3) expressions were tested respectively. Then, si-HIF1α was transfected into H9c2 cells to probe whether up-regulation of HIF1α attended to the influences of baicalin on hypoxia-stimulated H9c2 cells. Finally, the regulatory effect of nuclear factor E2-related factor 2 (Nrf2)/heme oxygenase 1 (HO-1) pathway on HIF1α expression was analyzed. Results: Hypoxia exposure aroused H9c2 cell viability reduction and apoptosis. Baicalin mitigated H9c2 cell viability reduction and apoptosis aroused by hypoxia. Moreover, HIF1α/BNIP3 pathway was further activated by baicalin in hypoxia-exposed H9c2 cells. Silencing HIF1α lowered the functions of baicalin on hypoxia-exposed H9c2 cells. Besides, baicalin enhanced hypoxia-caused activation of Nrf2/HO-1 pathway. Activation of Nrf2/HO-1 pathway was associated with the up-regulation of HIF1α and protective functions of baicalin on hypoxia-exposed H9c2 cells. Conclusion: Baicalin relieved cardiomyocytes H9c2 apoptosis aroused by hypoxia might be achieved through activating Nrf2/HO-1-mediated HIF1α/BNIP3 pathway. Highlights Baicalin mitigates H9c2 cell viability loss and apoptosis aroused by hypoxia; Baicalin activates HIF1a/BNIP3 pathway in hypoxia-exposed H9c2 cells; Silencing HIF1α weakens the influences of baicalin on hypoxia-exposed H9c2 cells; Baicalin promotes Nrf2/HO-1 pathway in hypoxia-exposed H9c2 cells; Promotion of Nrf2/HO-1 pathway is related to the up-regulation of HIF1α.

In this paper, we present our study on the effect of atractylenolide II on hyperlipidemic model mice. After 8 weeks, the blood of these mice was taken to detect four lipids. Pathological changes were detected in the aortas and livers of the mice. Expression of PPARα and SREBP-1C was detected in the liver by western blot. An enzyme-linked immunosorbent assay was used to detect the effects of atractylenolide II on blood lipids in hyperlipidemia mice. Hematoxylin and eosin staining was used to detect pathological changes in the aortas and livers of mice with hyperlipidemia after treatment with atractylenolide II. Changes in PPARα and SREBP-1C expression were found in mice with dyslipidemia. As the results shown, atractylenolide II administration reduced body weight and hyperlipidemia in hyperlipidemic model mice. In addition, atractylenolide II effectively relieved fat deposition and damage in aortic and liver tissues. Therefore, atractylenolide II had a beneficial therapeutic effect in reducing hyperlipidemia in hyperlipidemic model mice, which may be related to its ability to inhibit SREBP-1C expression by activating PPARα. The molecular mechanism driving the therapeutic effect of atractylenolide II may involve upregulation of PPARα and activation of the AMPK/PPARα/SREBP-1C signaling pathway. Our research demonstrated the development of therapeutic agents that can be used to improve hyperlipidemia.

Recently, a novel heterozygous missense mutation c.T1421G (p. L474R) in the PODXL gene encoding podocalyxin was identified in an autosomal dominant focal segmental glomerulosclerosis (AD-FSGS) pedigree. However, this PODXL mutation appeared not to impair podocalyxin function, and it is necessary to identify new PODXL mutations and determine their causative role for FSGS. In the present study, we report the identification of a heterozygous nonsense PODXL mutation (c.C976T; p. Arg326X) in a Chinese pedigree featured by proteinuria and renal insufficiency with AD inheritance by whole exome sequencing (WES). Total mRNA and PODXL protein abundance were decreased in available peripheral blood cell samples of two affected patients undergoing hemodialysis, compared with those in healthy controls and hemodialysis controls without PODXL mutation. We identified another novel PODXL heterozygous nonsense mutation (c.C1133G; p.Ser378X) in a British–Indian pedigree of AD-FSGS by WES. In vitro study showed that, human embryonic kidney 293T cells transfected with the pEGFP-PODXL-Arg326X or pEGFP-PODXL-Ser378X plasmid expressed significantly lower mRNA and PODXL protein compared with cells transfected with the wild-type plasmid. Blocking nonsense-mediated mRNA decay (NMD) significantly restored the amount of mutant mRNA and PODXL proteins, which indicated that the pathogenic effect of PODXL nonsense mutations is likely due to NMD, resulting in podocalyxin deficiency. Functional consequences caused by the PODXL nonsense mutations were inferred by siRNA knockdown in cultured podocytes and podocalyxin down-regulation by siRNA resulted in decreased RhoA and ezrin activities, cell migration and stress fiber formation. Our results provided new data implicating heterozygous PODXL nonsense mutations in the development of FSGS.

To investigate the effects of autologous platelet-rich plasma (PRP) on burn wound and burn pain in rats. Rats were treated with high-temperature copper rod to induce skin burn. During treatment, the wound area of rats was recorded on days 0, 3, 7, 10, 14 and healing rates were calculated. After 14-day treatment, the paw withdrawal mechanical threshold (PWMT) as well as paw withdrawal thermal latency were measured. In addition, CD31 expression in burn wound was detected by immunohistochemistry. The contents of TNF-α and IL-1β in wound tissues were detected by ELISA. Moreover, the mRNA and protein expression levels of VEGF, MMP-9, and TGF-β1 in wound tissues were detected by RT-qPCR together with Western blot. Burn wound of rats in the PRP group gradually got better with a decreased wound area. Compared with the NS group, the wound area of the PRP group was significantly reduced and the healing rate was significantly increased. Meanwhile, PWMT of the rats in the PRP group was obviously increased compared with the NS group. Compared with the NS group, the rate of CD31-positive cells in the wound tissue of burned rats was increased; while the contents of TNF-α and IL-1β were significantly decreased after a subcutaneous injection of PRP. In addition, the mRNA and protein expression levels of VEGF, MMP-9, and TGF-β1 in the wound tissue of rats from PRP group were evidently increased. Autologous platelet-rich plasma not only shortened the healing time, but also relieved the burn pain.

Background In this study, we have investigated the potential regulatory mechanisms of IL‐35 to relieve lupus nephritis (LN) through regulating Janus kinase (JAK)/signal transducers and activators of transcription (STAT) signaling pathway in mesangial cells. Results Among 105 significant differentially expressed proteins (DEPs) between juvenile systemic lupus erythematosus (JSLE) patients with LN and healthy controls, LAIR1, PDGFRβ, VTN, EPHB4, and EPHA4 were downregulated in JSLE‐LN. They consist of an interactive network with PTPN11 and FN1, which involved in IL‐35‐related JAK/STAT signaling pathway. Besides, urinary LAIR1 was significantly correlated with JSLE‐LN clinical parameters such as SLEDAI‐2K, %CD19+ B, and %CD3+ T cells. Through bioinformatics analysis of co‐immunoprecipitation with mass spectrometry results, including GO, KEGG, and STRING, five genes interacted with Lair1 were upregulated by IL‐35, but only Myh10 was downregulated. Therefore, we presumed an interactive network among these DEPs, JAK/STAT, and IL‐35. Moreover, the downregulated phosphorylated (p)‐STAT3, p‐p38 MAPK, and p‐ERK, and the upregulated p‐JAK2/p‐STAT1/4 in IL‐35 overexpressed mesangial cells, and RNA‐sequencing results validated the potential regulatory mechanisms of IL‐35 in alleviating JSLE‐LN disease. Moreover, the relieved histopathological features of nephritis including urine protein and leukocyte scores, a decreased %CD90+αSMA+ mesangial cells and pro‐inflammatory cytokines, the inactivated JAK/STAT signals and the significant upregulated Tregs in spleen, thymus and peripheral blood were validated in Tregs and IL‐35 overexpression plasmid‐treated lupus mice. Conclusions Our study provided a reference proteomic map of urinary biomarkers for JSLE‐LN and elucidated evidence that IL‐35 may regulate the interactive network of LAIR1‐PTPN11‐JAK‐STAT‐FN1 to affect JAK/STAT and MAPK signaling pathways to alleviate inflammation in JSLE‐LN. This finding may provide a further prospective mechanism for JSLE‐LN clinical treatment., A reference proteomic map of urinary biomarkers contributes to the diagnosis of JSLE‐LN. IL‐35 may interact with LAIR1‐PTPN11‐JAK‐STAT‐FN1 to affect JAK/STAT and MAPK signaling pathways to alleviate inflammation in vivo and in vitro. LAIR1 could be a novel potential target of IL‐35‐regulated JAK/STAT signaling pathway in JSLE‐LN.

Background. Hyperlipidemia, due to the practice of unhealthy lifestyles of modern people, has been a disturbance to a large portion of population worldwide. Recently, several scholars have turned their attention to Chinese medicine (CM) to seek out a lipid-lowering approach with high efficiency and low toxicity. This study aimed to explore the mechanism of Huatan Jiangzhuo decoction (HTJZD, a prescription of CM) in the treatment of hyperlipidemia and to determine the major regulation pathways and potential key targets involved in the treatment process. Methods. Data on the compounds of HTJZD, compound-related targets (C-T), and known disease-related targets (D-T) were collected from databases. The intersection targets (I-T) between C-T and D-T were filtered again to acquire the selected targets (S-T) according to the specific index. Gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment, as well as network construction, were applied to predict the putative mechanisms of HTJZD in treating hyperlipidemia. Thereafter, an animal experiment was conducted to validate the therapeutic effect of HTJZD. In addition, regulated differentially expressed genes (DEGs) were processed from the RNA sequencing analysis results. Common genes found between regulated DEGs and S-T were analyzed by KEGG pathway enrichment to select the key targets. Lastly, key targets were validated by real-time quantitative reverse transcription PCR (qRT-PCR) analysis. Results. A total of 210 S-T were filtered out for enrichment analysis and network construction. The enrichment results showed that HTJZD may exert an effect on hyperlipidemia through the regulation of lipid metabolism and insulin resistance. The networks predict that the therapeutic effect of HTJZD may be based on the composite pharmacological action of these active compounds. The animal experiment results verify that HTJZD can inhibit dyslipidemia in rats with hyperlipidemia, suppress lipid accumulation in the liver, and reverse the expression of 202 DEGs, which presented an opposite trend in the model and HTJZD groups. Six targets were selected from the common targets between 210 S-T and 202 regulated DEGs, and the qRT-PCR results showed that HTJZD could effectively reverse Srebp-1c, Cyp3a9, and Insr mRNA expression (P

Background: To identify new markers of juvenile systemic lupus erythematosus (JSLE) that facilitate patient stratification and prognosis is quite important. Therefore, our aim of the present study is to analyze alteration of protein expression and potential valuable biomarkers in juvenile systemic lupus erythematosus (JSLE) urine. Methods: Based on this aim, proteomics assay analyzed the changes of urinary proteins in study groups consisting of 9 healthy controls, 9 inactive JSLE and 10 active JSLE patients. And the correlationship between clinical characteristics of JSLE patients and new biomarkers discovered from proteomics assay was qualified.Results: We have identified a group of 105 differentially expressed proteins with ≥1.3 fold up-regulation or ≤0.77 fold down-regulation in JSLE patients. In gene ontology and functional enrichment analysis, we discovered these proteins were involved in several important biological processes such as acute phase inflammatory responses, complement activation, hemostasis, and immune system regulation. Interestingly, we found that Ephrin type-A receptor 4 (EPHA4) and Vitronectin (VTN) were significantly reduced in the urine of both inactive and active JSLE patients. Especially, the urinary VTN was also linear correlated with clinical characteristics of JSLE. Conclusion: In summary, this study provided a reliable proteomic reference profile for JSLE. Patients with active and inactive JSLE have differentially obvious metabolic proteins in the urine. VTN could be a specific diagnostic biomarker to distinguish inactive and active JSLE. These identified proteins as new biomarkers in this study can warrant some further exploiting in a larger prospective validation study.

Background: Early acute kidney injury (AKI) predicts a high mortality rate in severely burned patients. However, the pathophysiology of early AKI induced by severe burn has not been well-defined. This study was designed to examine the protective effects of calcium dobesilate (CaD) against severe burn-induced early AKI in mice and explore the mechanism. Methods: The shaved backs of mice were immersed in 100°C water for 10 s to make severe burn (40% of the total body surface area). CD-57 male mice were randomly divided into sham, burn, burn + vehicle, and burn + CaD groups. Renal function, reactive oxygen species generation, tubular necrosis, and phosphorylation of mitogen-activated protein kinase, protein kinase B (Akt), and nuclear factor (NF)-κB were measured at 24 and 48 h after the burn. Renal histology, ELISA, qRT-PCR, and Western blotting were performed on the renal tissue of mice to examine the effects and mechanisms at 24 and 48 h after the burn. Results: Tubular damage, cast formation, and elevations of serum creatinine, BUN, and renal tissue kidney injury molecule 1 levels were all observed in the burned mice, and these were all alleviated in the mice with CaD treatment. In addition, the levels of oxidation-reduction potential and malondialdehyde were decreased, while the activities of the endogenous antioxidative enzymes were increased in the kidney tissues from the mice after CaD treatment. Furthermore, the activities of Akt, p38, extracellular sign-regulated kinase, Jun N-terminal kinase, and NF-κB signaling were increased in the kidney of burned mice and normalized after CaD treatment. Conclusion: This study has established, for the first time, the protective effect of CaD against early AKI in severely burned mice. CaD may exert its protective effect through alleviating oxidative stress, apoptosis, and inflammation, as well as modulating some signaling pathways in the kidney.

A novel polymeric monolith using N,N-dimethylaminoethyl methacrylate as the monomer and ethylene glycol dimethacrylate as the crosslinker was successfully synthesized in a syringe and applied for direct solid-phase extraction of four benzodiazepines (bromazepam, triazolam, midazolam and diazepam) from undiluted urine samples prior to high performance liquid chromatography. The monolith was characterized by scanning electron microscopy, Fourier transform infrared spectroscopy and nitrogen adsorption-desorption experiments. Moreover, extraction parameters, including loading, washing and eluting conditions were optimized. Under the optimized conditions, the proposed method obtained linear ranges of 2.0-500 ng mL-1 with correlation coefficients (r) higher than 0.9997. The limits of detection (S/N = 3) and limits of quantification (S/N = 10) were 0.4-0.6 ng mL-1 and 1.4-2.0 ng mL-1, respectively. The recoveries at three spiked levels ranged from 83.7% to 103% with the intra- and inter-day precisions from 0.6-7.6% to 2.7-9.8%. The present monolith allowed direct loading of crude urine samples without any filtration or dilution step. Besides, the sorbent offered an enhancement factor of 16.7-20.6 and was stable enough for ten replicate cycles of extraction/desorption of urine samples. The developed method presented an alternative strategy for the accurate and convenient determination of benzodiazepines in urine samples.

Spinal cord decellularized (DC) scaffolds can promote axonal regeneration and restore hindlimb motor function of spinal cord defect rats. However, scarring caused by damage to the astrocytes at the margin of injury can hinder axon regeneration. Olfactory ensheathing cells (OECs) integrate and migrate with astrocytes at the site of spinal cord injury, providing a bridge for axons to penetrate the scars and grow into lesion cores. The purpose of this study was to evaluate whether DC scaffolds carrying OECs could better promote axon growth. For these studies, DC scaffolds were cocultured with primary extracted and purified OECs. Immunofluorescence and electron microscopy were used for verification of cells adhere and growth on the scaffold. Scaffolds with OECs were transplanted into rat spinal cord defects to evaluate axon regeneration and functional recovery of hind limbs. Basso, Beattie, and Bresnahan (BBB) scoring was used to assess motor function recovery, and glial fibrillary acidic protein (GFAP) and NF200-stained tissue sections were used to evaluate axonal regeneration and astrological scar distribution. Our results indicated that spinal cord DC scaffolds have good histocompatibility and spatial structure, and can promote the proliferation of adherent OECs. In animal experiments, scaffolds carrying OECs have better axon regeneration promoting protein expression than the SCI model, and improve the proliferation and distribution of astrocytes at the site of injury. These results proved that the spinal cord DC scaffold with OECs can promote axon regeneration at the site of injury, providing a new basis for clinical application.

Huatan Jiangzhuo decoction (HJD) is a combination of six traditional Chinese medicines that were used for lipid metabolism-related disorders, but its efficacy and underlying mechanisms have not been explored by modern research strategies. This study aimed to investigate the therapeutic role of HJD in determining the transcriptome level. Hyperlipidemia model was established by feeding Sprague-Dawley rats with high-fat diet. Differentially expressed genes (DEGs) were detected by high-through transcriptome sequencing, followed by gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis. The total cholesterol (TC) and triglyceride (TG) levels in hyperlipidemia model rats were significantly increased, whereas high-density lipoprotein (HDL) concentration decreased when compared to normal rats, and HJD significantly downregulated TC concentrations and liver coefficient in the hyperlipidemia rats. Histology staining showed that HDJ greatly recovered the lipid accumulation in rat hepatic stellate cells and aortic arch vascular wall thickness of hyperlipidemia rats. One thousand nine hundred and thirty-six DEGs were identified in the HJD-treated hyperlipidemia rats, which were associated with various biological processes and signaling pathways such as peroxisome proliferator-activated receptors, AMP-activated Protein Kinase , and insulin signaling pathways. Quantitative reverse transcription-polymerase chain reaction further confirmed the downregulated expression of cholesterol 7-α-hydroxylase(CYP7A1), liver orphan receptor(LXRα),peroxisome proliferator-activated receptor gamma(PPARγ),andSterol Response Element-Binding Protein 1c(SREBP1c) genes in hyperlipidemia rats treated with HJD. Our data first elucidated the gene expression profile of high-fat diet-induced hyperlipidemia in rats after HJD treatment, and lipid metabolism-related genes (CYP7A1, LXRα, PPARγ, and SREBP1c) may be potentially biomarkers for HJD-alleviated hyperlipidemia.

Several Cryptosporidium species that infect reptiles, especially squamates, are well described, but there is limited data about Cryptosporidium species infecting crocodilians. In this study, we assess the occurrence of intestinal parasites using traditional microscopic examination and describe the prevalence and Cryptosporidium species in the captive-bred Chinese alligators (Alligator sinensis) in eastern China using molecular methods. The results of microscopic examination showed that no intestinal parasites were detected among the 491 fecal samples examined from the Chinese alligators. The overall prevalence for Cryptosporidium was 0.41% (2/491) by PCR detection using the SSU rRNA locus. Sequence and phylogenetic analysis of the SSU rRNA, COWP, and actin genes revealed the presence of Cryptosporidium testudinis, which has been isolated primarily from chelonians. This is the first detection of the specific DNA of C. testudinis in the feces of the Chinese alligator. This study expands our knowledge of the Cryptosporidium species involved in crocodiles, and more extensive studies are necessary to confirm the validity of C. testudinis in crocodiles.

Background This investigation aimed to evaluate the role of methylation in the regulation of microRNA (miR)-122, miR-125b and miR-106b gene expression and the expression of their target genes during isoniazid (INH)-induced liver injury. Methods Rats were given INH 50 mg kg− 1·d− 1 once per day for 3, 7, 10, 14, 21 and 28 days and were sacrificed. Samples of blood and liver were obtained. Results We analysed the methylation and expression levels of miR-122, miR-125b and miR-106b and their potential gene targets in livers. Liver tissue pathologies, histological scores and alanine aminotransferase (ALT) and aspartate aminotransferase (AST) activities changed, indicating the occurrence of liver injury. Relative expression levels of miR-122, miR-125b and miR-106b genes in the liver decreased after INH administration and correlated with the scores of liver pathology and serum AST and ALT activities, suggesting that miR-122, miR-125b and miR-106b are associated with INH-induced liver injury. The amount of methylated miR-122, miR-125b and miR-106b in the liver increased after INH administration and correlated with their expression levels, suggesting the role of methylation in regulating miRNA gene expression. Two miR-122 gene targets, cell cycle protein G1 (Cyclin G1) and cationic amino acid transporter-1 (CAT-1), also increased at the mRNA and protein levels, which suggests that lower levels of miR-122 contribute to the upregulation of Cyclin G1 and CAT-1 and might play a role in INH-induced liver injury. Signal transducer and activator of transcription 3 (STAT3) was a common target gene of miR-125b and miR-106b, and its expression levels of mRNA and protein increased after INH administration. The protein expression of phosphorylated (p)-STAT3 and the mRNA expression of RAR-related orphan receptor gamma (RORγt) regulated by p-STAT3 also increased. Meanwhile, the mRNA and protein expression of interleukin (IL)-17 regulated by RORγt, and the mRNA and protein expression of CXCL1 and MIP-2 regulated by IL-17 increased after INH administration. These results demonstrate that lower levels of hepatic miR-125b and miR-106b contribute to the upregulation of STAT3 in stimulating the secretion of inflammatory factors during INH-induced liver injury. Conclusions Our results suggested that DNA methylation probably regulates the expression of miRNA genes (miR-122, miR-125b, and miR-106b), affecting the expression of their gene targets (Cyclin G1, CAT-1, and STAT3) and participating in the process of INH-induced liver injury. Electronic supplementary material The online version of this article (10.1186/s40360-018-0201-x) contains supplementary material, which is available to authorized users.

Objectives: The aim of the study was to examine the association of CHADS2/CHA2DS2-VASc scores with left atrial thrombus (LAT) and spontaneous echocardiographic contrast (SEC) in non-anticoagulated nonvalvular atrial fibrillation (NVAF) spontaneous patients, and to develop a new scoring system for LAT/SEC prediction. Methods: Consecutive non-anticoagulated NVAF patients with or without LAT/SEC by transesophageal echocardiography were identified in the Guangdong General Hospital. Results: Among 2,173 patients, the prevalence of LAT/SEC was 4.9%. Both predictive values of CHADS2 and CHA2DS2-VASc scores for the presence of LAT/SEC were low-to-moderate (receiver operating characteristic [ROC] = 0.591 and 0.608, respectively, p = 0.90). By multivariate analysis, non-paroxysmal AF, decreased left ventricular ejection fraction, and left atrial enlargement were positively associated with LAT/SEC, while CHADS2/CHA2DS2VASc scores were not. A new scoring system based on these 3 factors above significantly improved the discrimination for LAT/SEC (ROC = 0.792). Conclusions: CHADS2/CHA2DS2-VASc scores had limited value in predicting LAT/SEC; a new scoring system that combines AF type and echocardiographic parameters may better predict LAT/SEC as a surrogate for cardioembolic risk in NVAF patients.

This study explores the mechanism of histone acetylation under the effect of oxidative stress in rat liver injury induced by isoniazid (INH). Fifty-six adult SD rats were selected and divided randomly into INH groups (48) and control (8). Rats in INH groups were intragastrically injected with 55 mg kg-1 day-1 for 3, 7, 10, 14, 21, and 28 days, and control rats were given an equal volume of distilled water. Pathological changes in liver tissues were observed by HE staining. Western blot analysis was conducted to measure the expression levels of H3k14ac and H4k8ac. The activities of HAT, HDAC and IL-1β, and TNF-α were detected by ELISA in liver tissues. Real-time RT-PCR analysis was performed to determine the protein expression levels of HAT, HDAC, and IL-1β and the mRNA expression of TNF-α. The levels of superoxide dismutase (SOD) and malondialdehyde (MDA) were assayed by biochemical methods in liver tissues. At different time points, the SOD activity decreased, whereas the MDA content significantly increased after 14 days (FSOD = 11.15, FMDA = 7.42, P < 0.01). During this period, the expression of histone acetylated H3K14 and H4K8 acetylation decreased compared with the control group (FH3K14 = 4.18, FH4K8 = 3.87, P < 0.05); by contrast, HDAC1 and HDAC2 showed a high expression level compared with those in the control group (FHDAC1 = 29.13, FHDAC2 = 58.34, P < 0.01). Moreover, the expression of CBP/P300 was lower than that in the control group (FCBP/P300 = 12.18, P = 0.001), and the protein contents of IL-1β and TNF-α in rat liver tissues were up-regulated (FIL-1β = 44.88, FTNF-α = 41.56, P < 0.01). These results suggest that histone acetylation is involved in INH-induced rat liver injury. Furthermore, the hypoacetylation of histones H3K14 and H4K8 is negatively correlated with oxidative stress-mediated rat liver injury.

Anaerobic ammonium oxidation (anammox) process exhibits advantages in treating high-ammonium livestock wastewater, while the anammox bacteria is vulnerable to heavy metal and antibiotics. Arsenic and sulfonamides extensively existed in livestock wastewater; unfortunately, their effects on the anammox process have not yet been investigated. This work comprehensively evaluated the single and joint effects of As(III) and sulfamethoxazole (SMX) on the anammox process and revealed the related inhibitory mechanism. Anammox had extraordinary resistance to As(III) stress (0–50 mg L−1), while nitrogen removal sharply deteriorated under the stress from 50 mg L−1 As(III) and 3 mg L−1 SMX. Exogenous As(III) damaged the protection of extracellular polymeric substance (EPS) and aggravated the inhibition of SMX. As(III) had direct toxic effects on anammox bacteria, while enhanced denitrifying capacity was the reason for inhibition of anammox by SMX. Moreover, the host arsenic resistance genes were changed under SMX inhibition. The findings of this study enrich our knowledge of the anammox response to various pollutants, and provide the operational guidance for anammox process to treat wastewater containing antibiotic and heavy metal.

The aim of this study was to investigate the difference in resistance mechanisms and fitness of Salmonella Typhimurium (ST) and Salmonella Enteritidis (SE) mutants selected during the evolution of resistance under exposure to increasing ciprofloxacin concentrations in vitro. Mutations in quinolone target genes were screened by PCR. Phenotypic characterization included susceptibility testing by the broth dilution method, investigation of efflux activity and growth rate, and determination of the invasion of human intestinal epithelium cells in vitro. The two Salmonella serotypes exhibited differences in target gene mutations and efflux pump gene expression during the development of resistance. In the parental strains, ST had a competitive advantage over SE. During the development of resistance, initially, the SE strain was more competitive. However, once ciprofloxacin resistance was acquired, ST once again became the more competitive strain. In the absence of bile salts or at 0.1% bile, the growth rate of SE was initially greater than that of ST, but once ciprofloxacin resistance was acquired, ST had higher growth rates. ST strains showed decreased invasion of epithelial cells in 0.1% bile. These data indicate that ciprofloxacin-resistant ST strains are more competitive than ciprofloxacin-resistant SE strains.

This study investigated the diagnostic value of 5-methylcytosine (5-mC) and 5-hydroxymethylcytosine (5-hmC) contents of human leucocyte antigen (HLA)-B and HLA-DQB1 in anti-tuberculosis drug-induced liver injury (ADLI). In total, 110 ADLI patients and 120 patients without ADLI controls were enrolled. Enzyme-linked immunosorbent assay (ELISA) was used to detect the 5-mC and 5-hmC content in DNA from peripheral blood leucocytes. The univariate analysis showed that smoking, drinking, and 5-mC and 5-hmC content of HLA-B and HLA-DQB1 were significantly associated with ADLI. After adjusting for drinking and smoking, we found that 5-mC content of HLA-B and HLA-DQB1 were associated with ADLI (odds ratio [OR] = 0.251 and 0.347, respectively) and 5-hmC contents of HLA-B and HLA-DQB1 were also associated with ADLI (OR = 1.848 and 4.705, respectively). Receiver operating characteristic (ROC) analysis indicated that the 5-hmC contents of both HLA-B and HLA-DQB1 were more clinically significant than the 5-mC contents were. The combined 5-hmC level of HLA-B and HLA-DQB1 was the best diagnostic biomarker for ADLI, with the highest areas under the curve (AUC) for 0.953, sensitivity for 0.900 and specificity for 0.875. Therefore, combined 5-hmC levels of HLA-B and HLA-DQB1 could be significant evidence for diagnosis of ADLI.

Background: Cardiomyocytes loss is the predominant pathogenic characteristic in the hypoxia-induced injury. Meanwhile, it has been corroborated that Bcl-2 E1B 19-KDa interacting protein 3 (BNIP3) p...

The Alisol A 24-acetate is an effective component of the Alismatis Rhizoma (AR) extract, which is often used in the treatment of hyperlipidemia. This study explored the effect and mechanism of the Alisol A 24-acetate from AR on lipid deposition in the liver of hyperlipidemic mice. After establishing hyperlipidemic mouse model (Model) by oral high-fat diet (HFD), the animals were treated with Alisol A 24-acetate for 4 weeks. The changes of blood lipid in mice were detected by ELISA. Hematoxylin and eosin (H&E) staining was used to evaluate the degree of liver lipid deposition in hyperlipidemic mice. Quantitative reverse transcriptase PCR (RT-qPCR) was used to detect the expression of ABCG1 and ABCA1 mRNA in the liver. The expression of ABCG1 and ABCA1 protein was detected by Western blotting (WB). After 4 weeks of high-fat diet, the levels of TC, TG, and LDL-C in the mouse were increased, and the HDL-C level was decreased. After treatment with Alisol A 24-acetate, the levels of TC, TG, and LDL-C in the blood of hyperlipidemic mouse were significantly reduced, and the level of HDL-C was increased. The results of H&E staining showed that the lipid deposition in the liver of hyperlipidemic mouse was improved after treatment with Alisol A 24-acetate. RT-qPCR and WB analysis documented that ABCG1 and ABCA1 mRNA and protein expression in hyperlipidemic mice were promoted after the Alisol A 24-acetate treatment. In conclusion, Alisol A 24-acetate effectively alleviates the liver lipid deposition in hyperlipidemic mice, and this effect is achieved mostly by promoting the expression of ABCG1 and ABCA1 at the mRNA and protein levels.

A sensitive, rapid and homogeneous reaction measurement method for quantitation of human epididymis protein 4 (HE4) in human serum by amplified luminescent proximity homogeneous immunoassay (AlphaLISA) was described. Built on a sandwich-type immunoassay format, analytes in samples were captured by one biotinylated monoclonal antibody combining on the surface of streptavidin coated donor beads, and "sandwiched" by another monoclonal antibody coated on acceptor beads. The coefficient variations of the method were lower than 10%, and the recoveries were in the range of 90-110% for serum samples. A value of 0.88pmol/l was identified as the minimum detectable dose of the present method for HE4. Compared with the results from electrochemiluminescence immunoassay kit (Roche) in 170 serum samples, there was a satisfied correlation coefficient of 0.984. The present assay demonstrated high sensitivity, wider effective detection range and excellent reproducibility for quantitation of HE4 can be useful for early screening and prognosis evaluation of patients with ovarian cancer.

Prognostic value of peripheral monocyte, as a member of inflammatory cells, was widely being investigated. The aim of this study was to evaluate the prognostic value of preoperative peripheral blood monocyte count for hepatocellular carcinoma (HCC) patients who underwent liver transplantation (LT) and the relationship between monocyte count and tumor-related characteristics. We retrospectively analyzed the clinical data of 101 HCC patients after LT. Preoperative monocyte count and demographic, clinical, and pathologic data were analyzed. The optimal cutoff value of monocyte count was 456/mm(3), with the sensitivity and specificity of 69.4 and 61.5 %, respectively. Elevated preoperative peripheral blood monocyte count was significantly associated with large tumor size. The 1-, 3-, and 5-year disease-free survival (DFS) (80.9, 70.1, and 53.3 % vs 55.1, 38.7, and 38.7 %, P = 0.007) and overall survival (OS) rates (95.7, 76.6, and 64.8 % vs 72.2, 44.1, and 36.1 %, P = 0.002) of HCC patients in the peripheral blood monocyte count ≤456/mm(3) group were higher than those in the peripheral blood monocyte count456/mm(3) group. In conclusion, elevated preoperative peripheral blood monocyte count was significantly associated with advanced tumor stage and it can be considered as a prognostic factor for HCC patients after LT.

Diacylglycerol kinase alpha (DGKA) functions as lipid kinase to phosphorylate the lipid diacylglycerol (DAG). DGKA has been characterized to negative regulate the Ras-MAPK pathway in T lymphocytes. A 2018 study using crispr knockouts of DGKA have shown the anti tumor activity of T-cells continue to increase in the presence of PD-L1 positive tumor cells. Little is known about the expression patterns of DGKA in human cancer. In our previous study, we explore the tumor micro environment with a number of immune cell markers such as CD3, CD8A, CD20, CD68, TIM3 and LAG3 with PD-L1 expression in melanoma, NSCLC, and bladder cancer and found a few unique signatures for these cancers. In this study, we evaluate expression pattern of DGKA in various cancers by immunohistochemistry to elucidate the signature profile of DGKA expression with PD-L1 and other markers in the PD-L1 tumor micro environment. Citation Format: Rachel M. Gonzalez, Tianli Qu, Xiaomin Hu, Qi Ren, Qiankun Zhang, Zhaoying Guo, Young-Hwan Kim, Yiran Wang, Xuan Liu, Wei Fu. PD-L1 and diacylglycerol kinase alpha (DGKA) expression in melanoma, nsclc and bladder cancers [abstract]. In: Proceedings of the Annual Meeting of the American Association for Cancer Research 2020; 2020 Apr 27-28 and Jun 22-24. Philadelphia (PA): AACR; Cancer Res 2020;80(16 Suppl):Abstract nr 4985.

We performed a meta-analysis to evaluate the outcomes of acute ischemic stroke (AIS) in patients treated with mechanical thrombectomy (MT), according to diabetes mellitus and admission glucose level (AGL). We systematically reviewed previous studies in PubMed that reported outcomes of MT in AIS patients and their relationships with diabetes mellitus or AGL. We used functional independence (modified Rankin score ≤ 2 at 3 months) as the primary end point. Data from 12,653 patients in 47 articles that evaluated the effect of diabetes mellitus or AGL on outcomes after MT were included. Compared with patients without a history of diabetes mellitus, patients with a diabetes mellitus history had significantly lower odds of functional independence in both the unadjusted meta-analysis (odds ratio [OR] 0.64; 95% confidence interval [CI] 0.54–0.75) and the multivariable analysis (OR 0.48; 95% CI 0.33–0.71). Similarly, higher AGL was associated with an unfavorable functional outcome in the unadjusted meta-analysis (pooled effect size − 0.38; 95% CI − 0.45 to − 0.31), and the adjusted OR (95% CI) per 1 mmol/L increase in AGL was 0.87 (0.83–0.92) for functional independence according to the combined multivariable results. Recanalization rate and symptomatic intracranial hemorrhage were neither related to AGL nor different in patients with or without diabetes mellitus. The present study confirms that a history of diabetes mellitus and high AGL are associated with unfavorable functional outcomes at 3 months after MT in AIS patients. However, the causal relationship between hyperglycemia and poor prognosis remains undetermined, and further investigations are required to ascertain whether AIS patients receiving MT could benefit from intensive glucose control.

Astragalus polysaccharide (APS) has been widely reported to play an important role in inflammatory response. In this study, we aimed to explore the effects and underlying mechanisms of APS on lipopolysaccharide (LPS)-induced inflammation injury in H9c2 cardiomyoblasts. H9c2 cells were treated with different concentrations of APS, and cell viability was detected by the Cell Counting Kit-8 (CCK-8) assay. Then, the effect of APS on cell viability and apoptosis induced by LPS was determined by CCK-8, flow cytometry, and western blot. The expression and release of inflammatory cytokines were evaluated by quantitative real-time polymerase chain reaction (qRT-PCR), western blot, and enzyme-linked immunosorbent assay (ELISA). Furthermore, expression of miR-127 in H9c2 cells was analyzed by qRT-PCR, and knocked down by transfection with miR-127 inhibitor. Western blot was used to analyze signaling pathway molecules. APS had no effect on H9c2 cells viability. However, APS could alleviate LPS-induced inflammation injury by increasing cell viability, reducing apoptosis, and inhibiting release of inflammatory cytokines in H9c2 cells ( P < 0.05). Additionally, we found that APS increased toll-like receptor 4 (TLR4) expressions in LPS-treated H9c2 cells. Mechanistically, we found that APS exerted the protective effect by down-regulating LPS-increased expression of miR-127 ( P < 0.05), inhibiting nuclear factor kappa B (NF-κB), JNK and promoting phosphoinositide 3-kinase/protein kinase B (PI3K/AKT) signaling pathways in LPS-treated H9c2 cells. The results demonstrated that APS could protect H9c2 cells against LPS-induced inflammation injury, which might be partially due to miR-127 down-regulation and regulation of NF-κB, JNK, and PI3K/AKT signaling pathways. These findings indicated that APS might be a potential therapeutic drug for treatment of myocarditis.