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Oxygen glucose deprivation/re-oxygenation (OGD/R)-mediated ischemia of kidney is frequently leads to enhanced apoptosis and amplified inflammatory response. Sappanchalcone (Sap) is a flavonoid compound that extracted from Caesalpinia sappan L. with a range of cell-protective activities. Herein, we primarily reconnoitered the influence of Sap in HK-2 cells under OGD/R treatment. In this research, the consequence revealed that Sap might linked with ischemia of kidney. Besides, Sap lessened OGD/R-mediated HK-2 cell injury by boosting cell viability, inhibiting apoptosis and inflammation. In addition, Sap hindered activation of the TNFRSF1A/NF-kB signaling. Moreover, upregulation of TNFRSF1A diminished the repressive influence of Sap on OGD/R-mediated apoptosis and inflammation. In conclusion, Sap declined the OGD/R-induced HK-2 cell injury by downregulation of TNFRSF1A/NF-kB signaling, thereby offered a theoretical basis for the handling of ischemia of kidney.

Background: Podocyte apoptosis and autophagy dysfunction have been considered to be one of the important causes of diabetic nephropathy (DN). Emodin has the function of regulating autophagy. The present study was performed to investigate the effect of emodin on high glucose (HG)-induced podocyte apoptosis and whether the potential anti-apoptotic mechanism of emodin is related to the induction of AMPK/mTOR-mediated autophagy in MPC5 cells in vitro.Methods: The viability and apoptosis of podocytes (MPC5 cells) were detected using CCK-8 assay, trypan blue exclusion assay and flow cytometry analysis, respectively. The expression levels of Cleaved caspase-3, autophagy maker LC3 I/II, and AMPK/mTOR signaling pathway-related proteins were evaluated with western blot analysis. The changes of morphology and RFP-LC3 fluorescence were observed under microscopy.Results: HG (20-160 mmol/L) dose-dependently induced cell apoptosis in MPC5 cells, whereas emodin (4 μmol/L) significantly ameliorated HG-induced cell apoptosis and caspase-3 cleavage. Emodin (4 μmol/L) significantly increased LC3-II levels and induced RFP-LC3-containing punctate structures in MPC5 cells. Furthermore, the protective effects of emodin were mimicked by rapamycin (100 nmol/L). Moreover, emodin increased the phosphorylation of AMPK and suppressed the phosphorylation of mTOR. The AMPK inhibitor compound C (10 μmol/L) abolished emodin-induced autophagy activation.Conclusion: Emodin ameliorated HG-induced apoptosis of MPC5 cells in vitro that involved induction of autophagy through the AMPK/mTOR signaling pathway, which might provide a potential therapeutic option for DN.