【摘要】 目的：探讨仙茅苷对高糖诱导的肾小管上皮细胞炎症反应的影响及分子机制。方法：肾小管上皮细胞HK-2随机分为正常对照组（Con）、高糖组（HG）、HG+仙茅苷低、中、高剂量组、HG+miR-NC组、HG+miR-1247-3p组、HG+仙茅苷+antimiR-NC组、HG+仙茅苷+anti-miR-1247-3p组；ELISA检测TNF-α、IL-6水平；流式细胞术检测细胞凋亡；RT-qPCR检测miR-1247-3p水平。结果：仙茅苷低、中、高剂量处理后，高糖诱导的肾小管上皮细胞培养液中IL-6、TNF-α水平随药物浓度的增加逐渐降低，细胞凋亡率逐渐降低，miR-1247-3p表达水平逐渐升高（P<0.05）。与HG+miR-NC组相比，miR-1247-3p过表达肾小管上皮细胞培养液中IL-6、TNF-α水平降低，细胞凋亡率降低（P<0.05）。下调miR-1247-3p表达可逆转仙茅苷对高糖诱导的肾小管上皮细胞炎症反应作用。结论：仙茅苷通过上调miR-1247-3p表达抑制高糖诱导的肾小管上皮细胞炎症损伤。更多还原

【Abstract】 Objective:To investigate effect of curculigoside on inflammatory response of renal tubular epithelial cells induced by high glucose and its molecular mechanism. Methods:Renal tubular epithelial cells HK-2 were randomly divided into normal control group(Con), high glucose group(HG), HG+curculigoside low, medium and high dose groups, HG+miR-NC group, HG+miR-1247-3p group, HG+curculigoside+anti-miR-NC group, HG+curculigoside+anti-miR-1247-3p group; ELISA was used to detect TNF-αand IL-6 levels; flow cytometry was used to detect cell apoptosis; RT-qPCR was used to detect miR-1247-3p level. Results:After treatment with low, medium and high doses of curculigoside, levels of IL-6 and TNF-α in culture medium of renal tubular epithelial cells induced by high glucose were decreased with the increase of drug concentration, apoptosis rate was gradually decreased, expression level of miR-1247-3p was gradually increased(P<0.05). Compared with HG+miR-NC group, levels of IL-6 and TNF-α in culture medium of renal tubular epithelial cells were decreased after miR-1247-3p was overexpressed, rate of cell apoptosis was decreased(P<0.05). Down-regulating expression of miR-1247-3p can reverse effect of curculigoside on inflammatory response of renal tubular epithelial cells induced by high glucose. Conclusion:Curculigoside inhibits inflammatory injury of renal tubular epithelial cells induced by high glucose by up-regulating expression of miR-1247-3p.更多还原