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表没食子儿茶素-3-没食子酸酯通过抑制糖尿病db/db小鼠的氧化应激减轻肾脏损伤。

Epigallocatechin-3-gallate Attenuates Renal Damage by Suppressing Oxidative Stress in Diabetic db/db Mice.

作者信息

Yang Xiu Hong, Pan Yu, Zhan Xiao Li, Zhang Bao Long, Guo Li Li, Jin Hui Min

机构信息

Division of Nephrology, Shanghai Pudong Hospital, Fudan University Pudong Medical Center, 2800 Gong Wei Road, Shanghai, China.

Division of Nephrology, Shanghai No. 9 People's Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.

出版信息

Oxid Med Cell Longev. 2016;2016:2968462. doi: 10.1155/2016/2968462. Epub 2016 Sep 6.

DOI:10.1155/2016/2968462
PMID:27698952
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5028863/
Abstract

Epigallocatechin-3-gallate (EGCG), extracted from green tea, has been shown to have antioxidative activity. In the present study, we evaluated the effect of EGCG on the kidney function in db/db mice and also tried to investigate the underlying mechanism of the renoprotective effects of EGCG in both animals and cells. EGCG treatment could decrease the level of urinary protein, 8-iso-PGF2a, and Ang II. Moreover, EGCG could also change the level of several parameters associated with oxidative stress. In addition, the protein expression levels of AT-1R, p22-phox, p47-phox, p-ERK1/2, p-p38 MAPK, TGF-1, and -SMA in diabetic db/db mice were upregulated, and all of these symptoms were downregulated with the treatment of EGCG at 50 and 100 mg/kg/d. Furthermore, the pathological changes were ameliorated in db/db mice after EGCG treatment. HK-2 cell-based experiments indicated that EGCG could inhibit the expression of MAPK pathways, which is the downstream effector of Ang II mediated oxidative stress. All these results indicated that EGCG treatment could ameliorate changes of renal pathology and delay the progression of DKD by suppressing hyperglycemia-induced oxidative stress in diabetic db/db mice.

摘要

表没食子儿茶素没食子酸酯(EGCG)是从绿茶中提取的,已被证明具有抗氧化活性。在本研究中,我们评估了EGCG对db/db小鼠肾功能的影响,并试图研究EGCG在动物和细胞中肾脏保护作用的潜在机制。EGCG治疗可降低尿蛋白、8-异前列腺素F2α和血管紧张素II的水平。此外,EGCG还可改变与氧化应激相关的几个参数的水平。此外,糖尿病db/db小鼠中AT-1R、p22-吞噬细胞氧化酶、p47-吞噬细胞氧化酶、磷酸化细胞外信号调节激酶1/2、磷酸化p38丝裂原活化蛋白激酶、转化生长因子-1和α-平滑肌肌动蛋白的蛋白表达水平上调,而在50和100mg/kg/d的EGCG治疗下,所有这些症状均下调。此外,EGCG治疗后db/db小鼠的病理变化得到改善。基于HK-2细胞的实验表明,EGCG可抑制丝裂原活化蛋白激酶途径的表达,该途径是血管紧张素II介导的氧化应激的下游效应器。所有这些结果表明,EGCG治疗可改善糖尿病db/db小鼠的肾脏病理变化,并通过抑制高血糖诱导的氧化应激来延缓糖尿病肾病的进展。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5733/5028863/c9eaaae07d89/OMCL2016-2968462.008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5733/5028863/051f2ff70417/OMCL2016-2968462.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5733/5028863/d77aeaddb896/OMCL2016-2968462.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5733/5028863/2eacbe3f531e/OMCL2016-2968462.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5733/5028863/6081e51d0aa9/OMCL2016-2968462.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5733/5028863/c49fcb291bf3/OMCL2016-2968462.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5733/5028863/d3d84217e221/OMCL2016-2968462.006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5733/5028863/a86afa64d8c1/OMCL2016-2968462.007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5733/5028863/c9eaaae07d89/OMCL2016-2968462.008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5733/5028863/051f2ff70417/OMCL2016-2968462.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5733/5028863/d77aeaddb896/OMCL2016-2968462.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5733/5028863/2eacbe3f531e/OMCL2016-2968462.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5733/5028863/6081e51d0aa9/OMCL2016-2968462.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5733/5028863/c49fcb291bf3/OMCL2016-2968462.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5733/5028863/d3d84217e221/OMCL2016-2968462.006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5733/5028863/a86afa64d8c1/OMCL2016-2968462.007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5733/5028863/c9eaaae07d89/OMCL2016-2968462.008.jpg

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