雷公藤多苷对高糖诱导人肾小管上皮细胞凋亡及 CXCL10/CXCR3 轴的影响.

Objective To investigate effects of tripterygium glycosides (TG) on the apoptosis of human renal tubular epithelial cells HK-2 induced by high glucose and the CXC chemokine ligand 10 (CXCL10)/CXC chemokine receptor 3 (CXCR3) axis. Methods Human renal tubular epithelial cells HK-2 were cultured in vitro and divided into the control group (culture medium containing 5.5 mmol/L glucose), the high glucose group (culture medium containing 25 mmol/L glucose) and the 12.5, 25 and 50 mg/L TG groups (culture medium containing 12.5, 25 and 50 mg/L TG and 25 mmol/L glucose, respectively). Methyl thiazolyl tetrazolium (MTT) method was used to detect the viability of HK-2 cells. Flow cytometry was used to detect the apoptosis of HK-2 cells. 2',7'-dichlorodi-hydrofluorescein diacetate method was used to detect reactive oxygen species (ROS) level of HK-2 cells. Xanthine oxidase method was used to detect superoxide dismutase (SOD) level of HK-2 cells. Enzyme-linked immunosorbent assay was used to detect levels of inflammatory factors of tumor necrosis factor-α (TNF-α) and transforming growth factor-β1 (TGF-β1) in HK-2 cells. Western blot assay was used to detect the expression of apoptotic proteins (Caspase-3, Caspase-9), CXCL10 and CXCR3 proteins in HK-2 cells. Results Compared with the control group, the HK-2 cell viability and SOD level were significantly reduced in the high glucose group, and the apoptosis rate, ROS, TNF- α, TGF- β1 levels and Caspase-3, Caspase-9, CXCL10, CXCR3 protein expression levels were significantly increased (P＜0.05). Compared with the high glucose group, the HK-2 cell viability and SOD level were significantly increased in the 12.5, 25 and 50 mg/L TG groups, and the apoptosis rate, ROS, TNF-α, TGF-β 1 levels and Caspase-3, Caspase-9, CXCL10, CXCR3 protein expression levels were significantly reduced, and high dose TG has better effect (P＜0.05). Conclusion TG can inhibit high glucose induced apoptosis, oxidative stress and inflammation of HK-2 cells, and its mechanism may be related to the inhibition of CXCL10/CXCR3 axis. [ABSTRACT FROM AUTHOR]