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目的探讨C肽对高糖下肾足细胞凋亡和肾病蛋白的影响。方法将肾足细胞分成4组:对照组(5 mmol/L葡萄糖)、高糖组(25 mmol/L葡萄糖,下同)、C肽组(高糖+C肽)、百日咳毒素(PTX)组(高糖+C肽+PTX),干预24 h后,Western blot检测磷脂酰肌醇3激酶(PI3K)、蛋白激酶B(Akt)和m TOR蛋白,免疫荧光法检测肾病蛋白,TUNEL一步法检测足细胞凋亡。结果 5 nmol/L C肽即能显著抑制高糖下足细胞m TOR的表达(P<0.01)。与对照组相比,高糖组PI3K、Akt和m TOR表达显著升高(P<0.05),肾病蛋白表达显著下降(P<0.01),足细胞凋亡显著增加(P<0.01);与高糖组相比,C肽能逆转高糖所致的上述变化(P<0.01),而PTX能消除或减弱C肽的上述逆转作用(P<0.05)。结论C肽可抑制高糖激活的足细胞PI3K-Akt-m TOR信号通路,并减少高糖所致的足细胞肾病蛋白减少和足细胞凋亡。
Objective To investigate the effect of C peptide on renal podocyte apoptosis and nephropathy under high glucose conditions. Methods The renal podocytes were divided into 4 groups: control group (5 mmol / L glucose), high glucose group (25 mmol / L glucose, the same below), C peptide group (high glucose + C peptide), pertussis toxin (PTX) (High glucose + C peptide + PTX). After intervention for 24 h, the expressions of PI3K, Akt and mTOR proteins were detected by Western blot. The nephropathy protein was detected by immunofluorescence and TUNEL assay Podiatric apoptosis. Results 5 nmol / L C peptide significantly inhibited m TOR expression in podocytes with high glucose (P <0.01). Compared with the control group, the expression of PI3K, Akt and m TOR were significantly increased (P <0.05), the expression of nephropathy protein was significantly decreased (P <0.01) and the podocyte apoptosis was significantly increased (P <0.01) C peptide could reverse the above changes caused by high glucose (P <0.01), while PTX could eliminate or weaken the above reversed effect of C peptide (P <0.05). Conclusion C-peptide can inhibit the PI3K-Akt-m TOR signaling pathway in podocytes with high glucose and decrease the high protein-induced podocyte nephropathy and podocyte apoptosis.