Morroniside Inhibits apoptosis and Oxidative Stress in High Glucose-Induced Renal Tubular Epithelial Cells by Upregulating MiR-25

Abstract

Objective: Morroniside has been shown to have anti-apoptotic and anti-oxidative stress effects, but its role in diabetic nephropathy (DN)-related cell injury is still unclear. This study aims to explore the role and mechanism of morroniside in DN progression. Methods: Human renal tubular epithelial cells (HK2) were cultured with high glucose (HG) and treated with morroniside. Cell proliferation and apoptosis were measured by cell counting kit 8 method and flow cytometry. Western blot was used to detect the protein levels of apoptosis marker Bax and anti-apoptosis marker Bcl-2. Malonaldehyde (MDA) and superoxide dismutase (SOD) levels were examined to evaluate cell oxidative stress, and miR-25 expression was determined by quantitative real-time PCR. Results: After treated with HG, cell viability, Bcl-2 level, SOD activity and miR-25 expression were decreased, whereas apoptosis rate, Bax level and MDA content were increased. Morroniside enhanced cell viability, Bcl-2 level, SOD activity and miR-25 expression, while reduced apoptosis rate, Bax level and MDA content in HG-induced HK2 cells. Overexpression of miR-25 promoted cell viability, repressed HG-induced HK2 cell apoptosis and oxidative stress. Knockdown of miR-25 reversed the effects of morroniside on the viability, apoptosis and oxidative stress in HG-induced HK2 cells. Conclusion: Morroniside could inhibit HG-induced HK2 cell injury via increasing miR-25 expression, confirming that morroniside might alleviate DN process.