依普利酮抑制细胞增殖拮抗急性环孢素A肾损伤的研究

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目的探讨盐皮质激素受体阻断剂依普利酮抑制细胞增殖拮抗环孢素A肾损伤的作用。方法经口灌服环孢素A(100 mg.kg-1.d-1),诱导小鼠急性肾脏损伤,给以依普利酮100 mg.kg-1.d-1治疗,d 10采血、摘取肾脏。放免法检测血清醛固酮水平,免疫组化检测增殖细胞核抗原(PC-NA)、纤连蛋白表达;RT-PCR、Western blot检测PCNA、FN、TGF-β1表达。结果血清醛固酮水平检测显示环孢素A组(318.83±95.72)ng.L-1较空白对照组(82.05±23.04)ng.L-1升高,依普利酮可明显抑制其分泌(149.50±36.20)ng.L-1。环孢素A组肾脏PCNA阳性细胞增多,纤连蛋白表达增强;PCNA、FN、TGF-β1蛋白及mRNA表达较空白对照组明显上调,依普利酮可抑制其表达。结论依普利酮可以抑制醛固酮的分泌、抑制细胞增殖,减轻环孢素A诱导的肾脏损伤。 Objective To investigate the effects of eplerenone, a blocker of mineralocorticoid receptor antagonist, on renal injury induced by CsA. Methods Acute kidney injury was induced in mice by oral administration of cyclosporine A (100 mg.kg-1.d-1), and received eplerenone 100 mg.kg-1.d-1, d 10 blood , Remove the kidneys. The level of serum aldosterone was detected by radioimmunoassay, PCNA and fibronectin were detected by immunohistochemistry. The expression of PCNA, FN and TGF-β1 were detected by RT-PCR and Western blot. Results Serum aldosterone level showed that the level of cyclosporin A (318.83 ± 95.72) ng.L-1 was higher than that of the blank control group (82.05 ± 23.04) ng.L-1, and that of eplerenone was significantly inhibited (149.50 ± 36.20) ng.L-1. The expression of PCNA, FN, TGF-β1 protein and mRNA in ciclosporin A group increased significantly compared with the blank control group, and eplerenone could inhibit the expression of fibronectin. Conclusion Eplerenone can inhibit the secretion of aldosterone, inhibit cell proliferation and alleviate cyclosporine A-induced renal damage.
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