Inhibitory effect of tea polyphenols on transforming growth factor-beta1 expression in rat with cyclosporine A-induced chronic nephrotoxicity.
Inhibitory effect of tea polyphenols on transforming growth factor-beta1 expression in rat with cyclosporine A-induced chronic nephrotoxicity.
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DOI：
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发表时间：
2004
影响因子：
8.2
通讯作者：
S. Shi;Shu-sen Zheng;C. Jia;You-fa Zhu;Hai Xie
中科院分区：
文献类型：
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作者：
S. Shi;Shu-sen Zheng;C. Jia;You-fa Zhu;Hai Xie
目的探讨茶多酚(TP)对环孢素A(CsA)慢性肾毒性大鼠模型转化生长因子β1(TGF-β1)表达的抑制作用。方法采用CsA慢性肾毒性大鼠模型，4组大鼠分别给予赋形剂（0.1 mL/kg/d sc）、TP（80 mg/kg/d ig）、CsA（15 mg/kg/d sc）和TP加CsA（CsA 15 mg/kg/d sc+TP 80 mg/kg/d，ig）。在治疗第28天结束时，分析血清和尿液的肌酐清除率，分析肾组织的病理学分析。采用RT-PCR、免疫组化、Western blot检测TGF-β1 mRNA及其蛋白表达。结果 与媒介物或 TP 处理的对照组相比，CsA 处理的大鼠肾脏 TGF-β1 mRNA 及其蛋白质的表达增加。与单独使用CsA治疗的动物相比，CsA联合TP治疗的动物肾功能和间质纤维化得到改善，肾TGF-β1 mRNA及其蛋白表达降低（P<0.05）。结论 TP能显着抑制环孢素慢性肾毒性大鼠模型肾脏TGF-β1的表达，提示TP降低肾脏TGF-β1的表达是保护肾功能和组织结构的机制之一。
AIM To investigate the inhibitory effect of tea polyphenols (TP) on the transforming growth factor-beta1 (TGF-beta1) expression in rat model of cyclosporine A (CsA)-induced chronic nephrotoxicity. METHODS The rat model of CsA-induced chronic nephrotoxicity was used, 4 groups of rats were respectively treated with vehicle (0.1 mL/kg/d sc), TP (80 mg/kg/d ig), CsA (15 mg/kg/d sc) and TP plus CsA (CsA 15 mg/kg/d sc+TP 80 mg/kg/d, ig). At the end of day 28 of treatment, serum and urine are analyzed for creatinine clearance, kidney tissue for pathologic analysis. The TGF-beta1 mRNA and its protein expression were detected by RT-PCR, immunohistochemistry, and Western blot. RESULTS CsA-treated rats had increased renal expression of TGF-beta1 mRNA and its protein, compared with the vehicle- or TP-treated controls. The renal function and interstitial fibrosis were ameliorated and renal expression of TGF-beta1 mRNA and its protein was decreased in animals treated with CsA plus TP, compared with animals treated with CsA alone (P<0.05). CONCLUSION TP significantly inhibits renal expression of TGF-beta1 in rat model of cyclosporine-induced chronic nephrotoxicity, suggesting that the decreased renal expression of TGF-beta1 exerted by TP is one of mechanisms to protect renal function and tissue structure.