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绿茶肽通过抑制小鼠体内的TGF-β/Smad信号通路改善糖尿病肾病。

Green tea peptides ameliorate diabetic nephropathy by inhibiting the TGF-β/Smad signaling pathway in mice.

作者信息

Chen Xuhui, Sun Lingli, Li Dongli, Lai Xingfei, Wen Shuai, Chen Ruohong, Zhang Zhenbiao, Li Qiuhua, Sun Shili

机构信息

School of Biotechnology and Health Sciences, Wuyi University, Jiangmen 529020, China.

Tea Research Institute, Guangdong Academy of Agricultural Sciences/Guangdong Provincial Key Laboratory of Tea Plant Resources Innovation & Utilization, Guangzhou 510640, China.

出版信息

Food Funct. 2022 Mar 21;13(6):3258-3270. doi: 10.1039/d1fo03615g.

DOI:10.1039/d1fo03615g
PMID:35234233
Abstract

Diabetic nephropathy (DN) is the most important cause of middle and late-stage chronic kidney disease. Green tea polypeptides are extracted from tea pomace, and exhibit various pharmacological effects. In this study, we analyzed the reno-protective effects of green tea peptides in diabetic db/db mice, and explored the underlying mechanisms. Peptide treatment for 5 weeks significantly reduced the blood glucose levels and other indices of diabetes, and alleviated renal injury measured in terms of blood creatinine, urea nitrogen and urinary albumin/urinary creatinine levels. Mechanistically, the green tea peptides downregulated p-Smad2/3, α-SMA, ZO-1 and vimentin proteins in the kidney tissues, and elevated Smad7. Thus, green tea peptides inhibited the deposition of ECM proteins by suppressing excessive activation of the TGF-β/Smad signaling pathway and reducing fibronectin levels. On the other hand, tea peptides ameliorated renal injury by inhibiting the production of inflammatory factors (iNOS and TNF-α) by suppressing the NF-κB signaling pathway. In addition, we confirmed the inhibitory effect of green tea peptides on the TGF-β/Smad signaling pathway in TGF-β1-stimulated HK-2 cells. Therefore, tea peptides can be considered as an effective candidate for alleviating DN.

摘要

糖尿病肾病(DN)是中晚期慢性肾脏病的最重要病因。绿茶多肽从茶渣中提取,具有多种药理作用。在本研究中,我们分析了绿茶多肽对糖尿病db/db小鼠的肾脏保护作用,并探究其潜在机制。连续5周给予多肽治疗可显著降低血糖水平及其他糖尿病指标,并减轻以血肌酐、尿素氮和尿白蛋白/尿肌酐水平衡量的肾损伤。机制上,绿茶多肽下调肾组织中p-Smad2/3、α-SMA、ZO-1和波形蛋白的表达,并上调Smad7。因此,绿茶多肽通过抑制TGF-β/Smad信号通路的过度激活和降低纤连蛋白水平来抑制细胞外基质蛋白的沉积。另一方面,茶多肽通过抑制NF-κB信号通路减少炎症因子(iNOS和TNF-α)的产生来改善肾损伤。此外,我们证实了绿茶多肽对TGF-β1刺激的HK-2细胞中TGF-β/Smad信号通路的抑制作用。因此,茶多肽可被视为缓解糖尿病肾病的有效候选物。

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