糖肾康对高糖诱导人肾小管上皮细胞分泌基质金属蛋白酶-9及其抑制剂-1的影响

目的探讨糖肾康防治糖尿病肾病的作用机制。方法将体外培养的人肾小管上皮细胞（HK-2）分为空白组、高糖诱导组（30 mmol/L D-葡萄糖）、对照组（30 mmol/L D-葡萄糖＋10%空白血清）和糖肾康低（30 mmol/L D-葡萄糖＋5%糖肾康药物血清）、中（30 mmol/L D-葡萄糖＋10%糖肾康药物血清）、高剂量组（30 mmol/L D-葡萄糖＋20%糖肾康药物血清）。药物干预24、48 h后,ELISA检测细胞培养上清液中基质金属蛋白酶-9（MMP-9）及其抑制剂-1（TIMP-1）的含量。结果 HK-2经高糖诱导后,MMP-9分泌显著减少,TIMP-1分泌显著增加,与空白组比较,差异有统计学意义（P〈0.05）;经糖肾康干预后,MMP-9含量显著上升,TIMP-1含量显著下降,与高糖诱导组比较,差异有统计学意义（P〈0.05）。结论糖肾康通过调控高糖诱导人肾HK-2纤维化因子的分泌,达到防治糖尿病肾病的目的。

Effects of Tangshenkang on MMP-9 and TIMP-1 of Human Renal Tubular Epithelial Cell HK-2 Induced by High Glucose

Objective To explore the mechanism of Tangshenkang in the prevention and treatment of diabetic nephropathy. Methods HK-2 cells were cultured in vitro and divided into control group, high glucose group （30 mmol/L D-glucose）, control group （30 mmol/L D-glucose＋10% animal serum）, and Tangshenkang drug-containing serum therapy groups （30 mmol/L D-glucose＋5%low concentration Tangshenkang, 30 mmol/L D-glucose＋10%middle concentration Tangshenkang, 30 mmol/L D-glucose＋20% high concentration Tangshenkang）. After 24 h and 48 h treatment, MMP-9 and TIMP-1 in cell cultural supernatant were observed by ELISA. Results MMP-9 of HK-2 cultured with high glucose was much decreased and TIMP-1 increased significantly than the control group, with statistical significance （P〈0.05）. TIMP-1 significantly decreased and MMP-9 increased in HK-2 cultured with high glucose plus Tangshenkang compared with those only induced by high glucose, with statistical significance （P〈0.05）. Conclusion Tangshenkang could regulate the secretion of fibrosis cell factor of HK-2 cell induced by high glucose, which may be one of the mechanisms in its treatment of diabetic nephropathy.