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过氧化物酶体增殖物激活受体(PPAR)γ激动剂具有多种生物效应。其中噻唑烷二酮类(TZDs)能够降低糖尿病大鼠和2型糖尿病患者尿微量白蛋白的排出,延缓糖尿病肾病的进展。一方面TZDs可通过降低血糖、血脂延缓糖尿病肾病的发展;另一方面还可直接诱导肾小球系膜细胞凋亡及抑制其增殖,抑制糖尿病肾病的发展。TZDs的肾脏保护机制可能独立于胰岛素增敏或降糖作用之外,而有二脂酰甘油(DAG)-蛋白激酶C(PKC)-细胞外信号调节激酶(ERK)和PKC-核因子(NF)-κB途径的参与。
Peroxisome proliferator-activated receptor (PPAR) gamma agonists have a variety of biological effects. Among them, thiazolidinediones (TZDs) can reduce the excretion of urinary albumin in diabetic rats and type 2 diabetic patients and delay the progression of diabetic nephropathy. On the one hand, TZDs can delay the development of diabetic nephropathy by lowering blood sugar and blood lipid; on the other hand, it can directly induce mesangial cell apoptosis and inhibit its proliferation, and inhibit the development of diabetic nephropathy. The renal protective mechanism of TZDs may be independent of insulin sensitization or hypoglycemic activity, with the addition of DAG-PKC-ERK and PKC-NF ) -κB pathway.