Hydrazinocurcumin Induced Autophagy and Affected Cell Proliferation by Downregulating the JAK/STAT3 Signaling Pathway in Skin Squamous Cell Carcinoma.

This study aims to investigate the relevant mechanism by which hydrazinocurcumin (HC) interferes with A431 cell autophagy by inhibiting the STAT3 signaling pathway. Different concentrations of HC are used to treat A431 cells to study the effects of HC on A431 cell proliferation and apoptosis. Real-time fluorescent quantitative polymerase chain reaction (PCR) is used to further explore the relationship of HC with the JAK signaling pathway and autophagy. Double immunofluorescence staining is used to detect the fluorescence localization of LC3 and STAT3 after HC treatment. With increasing HC concentrations, A431 cell viability decreases in a dose-dependent manner, and the apoptosis rate increases significantly. Laser confocal colocalization reveals that the fluorescence of labeled LC3 protein is significantly increased, and the fluorescence of labeled STAT3 is significantly reduced in this study. HC may induce autophagy in A431 cells and affect cell proliferation by downregulating the JAK/STAT3 signaling pathway.

Inflammation Disturbed the Tryptophan Catabolites in Hippocampus of Post-operative Fatigue Syndrome Rats via Indoleamine 2,3-Dioxygenas Enzyme and the Improvement Effect of Ginsenoside Rb1.

AIM: Post-operative fatigue syndrome (POFS) is a common complication that prolongs the recovery to normal function and activity after surgery. The aim of the present study was to explore the mechanism of central fatigue in POFS and the anti-fatigue effect of ginsenoside Rb1. METHOD: We investigated the association between inflammation, indoleamine 2,3-dioxygenase (IDO) enzyme, and tryptophan metabolism in the hippocampus of POFS rats. A POFS rat model was induced by major small intestinal resection. Rats with major small intestinal resection were administered ginsenoside Rb1 (15 mg/kg) once a day from 3 days before surgery to the day of sacrifice, or with saline as corresponding controls. Fatigue was assessed with the open field test (OFT) and sucrose preference test (SPT). ELISA, RT-PCR, Western blot, immunofluorescence, and high-performance liquid chromatography (HPLC) were used to test the inflammatory cytokines; p38MAPK, NF-κB/p65, and IDO enzyme expressions; and the concentrations of tryptophan, kynurenine, and serotonin, respectively. RESULT: Our results showed that POFS was associated with increased expressions of inflammatory cytokines and p38MAPK and higher concentrations of kynurenine and tryptophan on post-operative days 1 and 3; a lower serotonin level on post-operative day 1; and an enhanced translocation of NF-κB/p65 and the IDO enzyme on post-operative days 1, 3, and 5. Ginsenoside Rb1 had an improvement effect on these. CONCLUSION: Inflammatory cytokines induced by large abdominal surgery disturb tryptophan metabolism to cause POFS through the activation of the p38MAPK-NF-κB/p65-IDO pathway in the hippocampus. Ginsenoside Rb1 had an anti-fatigue effect on POFS by reducing inflammation and IDO enzyme.

Molecular mechanism of astragalus polysaccharide in alleviating insulin resistance in HepG2 cells / 预防医学

Objective@#To clarify the effect of astragalus polysaccharide （AP） on insulin resistance model of HepG2 cells induced by hyperinsulinemia and its underlying molecular mechanism in lipid metabolism and oxidative stress.@*Methods@#HepG2 cells were divided into three groups： the control group was treated without any intervention; the model group was treated with 200 μL cell culture medium containing 10-6 mol/L insulin for 48 hours to build an insulin resistance model; the AP group was treated with optimal concentration of AP based on an insulin resistance model. After 24 hours, the concentration of H2O2 and the expression of PPARγ in each group were detected. @*Results@#AP could improve the survival rate of insulin-resistant HepG2 cells in a dose-dependent manner. The highest survival rate of the cells was （118.26±1.17）% with 10 μM AP. The concentration of H2O2 in the AP group was （0.82±0.09） μM, which was lower than （1.30±0.16） μM in the model group （P<0.05）, but was close to （0.78±0.09） μM in the control group （P>0.05）. The relative mRNA expression of PPARγ in the AP group was 0.96±0.04, which was higher than 0.51±0.05 in the model group （P<0.05）, but was close to 1.00±0.11 in the control group （P>0.05）.@*Conclusions@#In the insulin resistance model in vitro, AP can significantly increase the cell survival rate, reduce intracellular H2O2 concentration, and promote the expression of PPARγ. The mechanism may be related to lipid metabolism.