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Background: Streptococcus mutans (S. mutans) contributes to caries. The biofilm formed by S. mutans exhibits greater resistance to drugs and host immune defenses than the planktonic form of the bacteria. The objective of this study was to evaluate the anti-biofilm effect of cordycepin from the perspective of metabolomics. Methods: The minimum inhibitory concentration (MIC) was determined to evaluate the antimicrobial effect of cordycepin on planktonic S. mutans. The 24-h biofilm was treated with 128 µg/mL of cordycepin for 10 min at the 8- or 20-h time points. Biofilm biomass and metabolism were assessed using crystal violet and MTT assays and cordycepin cytotoxicity was evaluated in human oral keratinocytes (HOK) using CCK-8 assays. The live bacterial rate and the biofilm volume were assessed by confocal laser scanning microscopy. Metabolic changes in the biofilm collected at different times during with cordycepin were analyzed by metabolomics and verified by quantitative real-time PCR. Results: The results showed that treatment with 128 µg/mL cordycepin reduced both the biomass and metabolic activity of the biofilm without killing the bacteria, and cordycepin at this concentration showed good biocompatibility. Metabolomics analysis showed that differentially abundant metabolites following cordycepin treatment were mainly related to purine and nucleotide metabolism. After immediate treatment with cordycepin, genes related to purine and nucleotide metabolism were downregulated, and the levels of various metabolites changed significantly. However, the effect was reversible. After continuing culture for 4 h, the changes in genes and most metabolites were reversed, although the levels of 2'-deoxyadenosine, 2'-deoxyinosine, and adenine remained significantly different. Conclusions: Cordycepin has the effect of anti-biofilm of S. mutans, mainly related to purine and nucleotide metabolism. [ABSTRACT FROM AUTHOR]

Pharmaceutical contaminants are causing great attention for the public people, urgently requiring to be eliminated from the environment. Herein, commercial pharmaceutical carbamazepine was chosen as a model to be degraded by a heterogeneous Fenton system using natural pyrite as catalyst. The catalyst was characterized by X‐ray diffraction apparatus, high‐resolution transmission electron microscopy, and X‐ray photoelectron spectroscopy. The elements composition and chemical states of pyrite changed significantly after the Fenton reaction, which promoted the production of active species in the electron transfer process. The degradation efficiency of carbamazepine (2.5 mg/L) can reach 99.71% after 30 min with 0.3 g/L of pyrite and 5 mM of H2O2, respectively. The reaction system was suitable for a wide range of pH (3–9). The environmental adaptability examination of pyrite showed that humic acid (HA) had inhibitory effects on the degradation of carbamazepine. While the changes of degradation efficiency of carbamazepine were inconspicuous in the presence of NO3− and SO42−, indicating strong anti‐interference to environment common anions. Free‐radical capturers suggested that hydroxyl radical (∙OH), superoxide radical (∙O2−), and singlet oxygen (1O2) participated in the degradation of carbamazepine. This research has offered a new strategy of "treating wastes with wastes" to use pyrite to remove emerging pollutants. [ABSTRACT FROM AUTHOR]

Apigenin displays antioxidant and anti-inflammatory effects. However, effects of apigenin magnesium (AM) complex on these aspects remain unknown. This study investigated the effects of AM complex on oxidative stress and inflammatory responses in hydrogen peroxide (H2O2)-induced rat hepatic stellate cells (HSCs). The antioxidant and anti-inflammatory effects of AM complex at concentrations of 0.625, 1.25, and 2.5 mg/mL were evaluated, comparing to HSCs treated by H2O2 alone. Cell viability, reactive oxygen species (ROS), the activity of superoxide dismutase (SOD), glutathione (GSH), malondialdehyde (MDA), nitric oxide (NO), interleukin 6 (IL-6), and nuclear factor-kappa B (NF-κB) levels were measured. Moreover, cell apoptosis, mRNA expression levels of transforming growth factor-β (TGF-β), NF-κB, and inducible nitric oxide synthase (iNOS) were assessed. AM complex significantly inhibited oxidative stress and inflammatory response at concentrations of 0.625, 1.25, and 2.5 mg/mL (IC50 = 1.679 mg/mL). AM complex elevated the survival rate of H2O2-treated HSCs and had no toxic effects on HSCs. AM complex also promoted SOD activity and GSH levels but suppressed ROS, MDA, and NO levels. Additionally, AM complex decreased IL-6 and NF-κB levels, gene expression of TGF-β, NF-κB, and iNOS, as well as induced apoptosis of HSCs. Data indicated that AM complex mitigated oxidative stress and inflammatory responses on H2O2-treated HSCs, suggesting that AM complex is a possible candidate for anti-hepatic diseases. Additional efforts, both in vivo and in humans, are required to assess of AM complex as a potential therapeutic drug in liver diseases. [ABSTRACT FROM AUTHOR]

With the development of science and technology, and development of artery bypass, methods such as cardiopulmonary cerebral resuscitation have been practiced in recent years. Despite this, some methods fail to promote or recover the function of tissues and organs, and in some cases, may aggravate dysfunction and structural damage to tissues. The latter is typical of ischemia-reperfusion (IR) injury. Lipid peroxidation mediated by free radicals is an important process of myocardial IR injury. Myocardial IR has been demonstrated to induce the formation of large numbers of free radicals in rats, which promotes the peroxidation of lipids within unsaturated fatty acids in the myocardial cell membrane. Markers of lipid peroxidation include malondialdehyde, superoxide dismutase and lactic dehydrogenase. Recent studies have demonstrated that N-acetylcysteine (NAC) is able to dilate blood vessels, prevent oxidative damage, improve immunity, inhibit apoptosis and the inflammatory response and promote glutathione synthesis in cells. NAC also improves the systolic function of myocardial cells and cardiac function, prevents myocardial apoptosis, protects ventricular remodeling and vascular remodeling, reduces opiomelanocortin levels in the serum and increases the content of nitric oxide in the serum, thus improving vascular endothelial function. Therefore, NAC has potent pharmacological activity; however, the relatively fast metabolism of NAC, along with its large clinical dose and low bioavailability, limit its applications. The present study combined NAC with medicinal activated carbons, and prepared N-acetylcysteine activated carbon sustained-release microcapsules (ACNACs) to overcome the limitations of NAC. It was demonstrated that ACNACs exerted greater effective protective effects than NAC alone on myocardial IR injury in rats. [ABSTRACT FROM AUTHOR]

Objective: To evaluate the inhibitory effect of cordycepin on oral cancer xenograft in nude mice and explore the underlying mechanisms., Methods: Sixteen BALB/c mice bearing subcutaneous human tongue squamous cell carcinoma (TSCC) TCA-8113 cell xenografts were randomized into model group and cordycepin treatment group for daily treatment with saline and cordycepin for 4 weeks. After the treatment, the tumor xenografts were dissected and weighed to assess the tumor inhibition rate. Histological changes in the heart, spleen, liver, kidney, and lung of the mice were evaluated with HE staining, and tumor cell apoptosis was examined using TUNEL staining; The expressions of Bax, Bcl-2, GRP78, CHOP, and caspase-12 in the xenografts were detected using RT-qPCR and Western blotting., Results: Cordycepin treatment resulted in a tumor inhibition rate of 56.09% in the nude mouse models, induced obvious changes in tumor cell morphology and significantly enhanced apoptotic death of the tumor cells without causing pathological changes in the vital organs. Cordycepin treatment also significantly reduced Bcl-2 expression ( P < 0.05) and increased Bax, GRP78, CHOP, and caspase-12 expressions at both the RNA and protein levels in the tumor tissues., Conclusion: Cordycepin treatment can induce apoptotic death of TCA-8113 cell xenografts in nude mice via the endogenous mitochondrial pathway and endoplasmic reticulum stress pathways.

Context: Apigenin displays antioxidant and anti-inflammatory effects. However, effects of apigenin magnesium (AM) complex on these aspects remain unknown. Objective: This study investigated the effects of AM complex on oxidative stress and inflammatory responses in hydrogen peroxide (H 2 O 2 )-induced rat hepatic stellate cells (HSCs). Materials and methods: The antioxidant and anti-inflammatory effects of AM complex at concentrations of 0.625, 1.25, and 2.5 mg/mL were evaluated, comparing to HSCs treated by H 2 O 2 alone. Cell viability, reactive oxygen species (ROS), the activity of superoxide dismutase (SOD), glutathione (GSH), malondialdehyde (MDA), nitric oxide (NO), interleukin 6 (IL-6), and nuclear factor-kappa B (NF-κB) levels were measured. Moreover, cell apoptosis, mRNA expression levels of transforming growth factor-β (TGF-β), NF-κB, and inducible nitric oxide synthase (iNOS) were assessed. Results: AM complex significantly inhibited oxidative stress and inflammatory response at concentrations of 0.625, 1.25, and 2.5 mg/mL (IC 50 = 1.679 mg/mL). AM complex elevated the survival rate of H 2 O 2 -treated HSCs and had no toxic effects on HSCs. AM complex also promoted SOD activity and GSH levels but suppressed ROS, MDA, and NO levels. Additionally, AM complex decreased IL-6 and NF-κB levels, gene expression of TGF-β, NF-κB, and iNOS, as well as induced apoptosis of HSCs. Discussion and conclusions: Data indicated that AM complex mitigated oxidative stress and inflammatory responses on H 2 O 2 -treated HSCs, suggesting that AM complex is a possible candidate for anti-hepatic diseases. Additional efforts, both in vivo and in humans, are required to assess of AM complex as a potential therapeutic drug in liver diseases.

Objective: To investigate the effect of apigenin on the protein expression levels of peroxisome proliferator-activated receptors (PPARs) in liver tissues of rats with nonalcoholic steatohepatitis (NASH)., Methods: The NASH rat model was established by feeding of a high-fat diet. Unmodeled rats served as the normal controls. The modeled rats were divided into a model control group, Essentiale treatment grouP(300 mg/kg/day),and three apigenin treatment groups for low-dose (15 mg/kg/day), moderate-dose (30 mg/kg/day) and high-dose (60 mg/kg/day). After 13 weeks of treatment,changes in insulin sensitivity from pre-treatment baseline were assessed by measuring the alanine aminotransferase (ALT), aspartate aminotransferase (AST),total cholesterol (TC),triglycerides (TG),low-density and high-density lipoprotein cholesterol (LDL-C and HDL-C),fasting blood glucose (FBG) and fasting insulin (FINS).The liver index and HOMA-IR were also calculated.Protein and gene expression of PPARα and PPARgamma in liver tissue were assessed by immunohistochemistry and RT-PCR.Statistical analysis was performed by the LSD test and Games-Howell test., Results: The apigenin-treated groups showed a significantly greater change in insulin sensitivity than the untreated model group,with the most significant change occurring in the high-dose grouP(P less than 0.05).Compared with the untreated model group,the apigenin-treated groups showed lower levels of ALT (95.4+/-7.3),AST (183.7+/-14.3),TC (1.61+/-0.25),TG (1.23+/-0.21),LDL-C (1.86+/-0.14),FBG (5.29+/-1.45) and FINS (0.76+/-0.86),but a higher level of HDL-C (1.04+/-0.17); again,the high-dose group showed the greatest change (all P less than 0.05).Compared to the untreated model group,the apigenin-treated groups showed significantly lower liver index (3.75+/-0.25 vs.2.90+/-0.17) and HOMA-IR (1.34+/-0.06 vs.0.18+/-0.04),with the high-dose group showing the greatest change (both P less than 0.05). Compared to the untreated model group,the apigenin-treated groups showed higher levels of protein and mRNA of PPARα (18.27+/-4.05 and 0.63+/-0.02,respectively) and PPARgamma(8.48+/-5.05 and 0.39+/-0.02),with the high-dose group showing the greatest change (all P < 0.05)., Conclusion: Apigenin can improve glucose tolerance,lipid metabolism and insulin resistance while decreasing blood levels of TC,TG,LDL-C,FBG,FINS and HOMA-IR,and increasing HDL-C in NASH,as shown in a high-fat diet induced rat model, and may have therapeutic potential.