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Journal of Tea Science ›› 2023, Vol. 43 ›› Issue (6): 784-794.doi: 10.13305/j.cnki.jts.2023.06.003

• Research Paper • Previous Articles     Next Articles

The Investigation of the Ameliorate Effect and Mechanism of EGCG on Non-obese GK Rat with Diabetic Kidney Damage

PENG Liyuan, ZENG Hongzhe, WAN Liwei, WEN Shuai, LIU Changwei, AN Qin, BAO Sudu, HUANG Jian'an*, LIU Zhonghua*   

  1. Key Lab of Education Ministry of Hunan Agricultural University for Tea Science, National Research Center of Engineering and Technology for Utilization of Botanical Functional Ingredients, Co-Innovation Center of Education Ministry for Utilization of Botanical Functional Ingredients, Key Laboratory for Evaluation and Utilization of Gene Resources of Horticultural Crops, Ministry of Agriculture and Rural Affairs of China, Changsha 410128, China
  • Received:2023-09-11 Revised:2023-11-05 Online:2023-12-15 Published:2024-01-08

Abstract: Epigallocatechin gallate (EGCG) is an antioxidant and anti-inflammatory natural active ingredient, and fewer studies have been conducted on the antioxidant and anti-inflammatory effects of EGCG in DKD and the regulatory mechanisms. This study investigated the effect and mechanism of EGCG on diabetic kidney damage in non-obese GK rats with idiopathic T2DM. Two different doses of EGCG (10 mg·kg-1 and 120 mg·kg-1) were administered to GK rats for 4 weeks. The body weight and daily food intake of rats were monitored during the experiment. At the end of the experiment, the serum and kidney tissues were collected to detect some kidney biochemical and pathological indicators and Nrf2-Keap1/MAPK signaling pathway related gene expression levels. The results show that EGCG could improve the kidney morphology and significantly increase the activities of antioxidant enzymes (such as SOD, CAT and GSH-Px), and inhibit the release of proinflammatory cytokines (MCP-1, IL-1β). In addition, EGCG could restrain oxidant stress by up-regulate the expression level of Nrf2 and inhibit inflammation by down-regulating the expression levels of JNK, NF-κB and P38 genes in kidney. The improvement effect of high dose was better than that of low dose in the experimental range. In conclusion, these results indicate that EGCG could ameliorate kidney injury caused by diabetes, and its mechanism might be related to anti-oxidative stress mediated by Nrf2-Keap1/MAPK signaling pathways.

Key words: EGCG, diabetic kidney damage, oxidant stress, inflammation, diabetes, GK rats

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