Journal
EXPERIMENTAL BIOLOGY AND MEDICINE
Volume 247, Issue 16, Pages 1410-1419Publisher
SAGE PUBLICATIONS LTD
DOI: 10.1177/15353702221106479
Keywords
Epigallocatechin-3-gallate; diabetic nephropathy; rat; endoplasmic reticulum stress; NOD-like receptor family pyrin domain containing 3 inflammasome; inflammation
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Funding
- Natural Science Research Project of Hefei Normal University [2021KJZD25]
- Natural Science Research Project of Bengbu Medical College [2020byzd033]
- Natural Science Research Project of Anhui Educational Committee [KJ2021A0697, KJ2021A0922]
- Anhui Provincial Natural Science Foundation [2008085MC65]
- Research Activities of Postdoctoral Researchers Foundation of Anhui Province [2020B470]
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This study revealed the protective effects of EGCG in type 2 diabetic kidneys, achieved by inhibiting the overactivation of ER stress-mediated NLRP3 inflammasome.
Epigallocatechin-3-gallate (EGCG), an essential polyphenolic constituent found in tea leaves, possesses various potent biological activities. This research was undertaken to investigate the impact of EGCG against endoplasmic reticulum (ER) stress-mediated inflammation and to clarify the underlying molecular mechanism in type 2 diabetic kidneys. The male rats were randomized into four groups: normal, diabetic, low-dose EGCG, and high-dose EGCG. In type 2 diabetic rats, hyperglycemia and hyperlipidemia noticeably caused renal structural damage and dysfunction and aggravated ER stress. Meanwhile, sustained ER stress activated the NOD-like receptor family pyrin domain containing 3 (NLRP3) inflammasome and then upregulated the contents of inflammatory cytokines in the diabetic kidney. Following supplementation with 40 mg/kg and 80 mg/kg EGCG, hyperglycemia, hyperlipidemia, and renal histopathological alterations and dysfunction were noticeably ameliorated; renal ER stress, NLRP3 inflammasome, and inflammatory response were markedly repressed in the EGCG treatment groups. In summary, the current study highlighted the renoprotective effects of EGCG in type 2 diabetes and its mechanisms are mainly associated with the repression of ER stress-mediated NLRP3 inflammasome overactivation.
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