School of Life Sciences, Hefei Normal University, Hefei 230601, China.
Anhui Province Key Laboratory of Medical Physics and Technology, Institute of Health & Medical Technology, Hefei Institutes of Physical Science, Chinese Academy of Sciences, Hefei 230031, China.
Exp Biol Med (Maywood). 2022 Aug;247(16):1410-1419. doi: 10.1177/15353702221106479. Epub 2022 Jul 1.
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.
没食子酸表没食子儿茶素酯(EGCG)是茶叶中一种重要的多酚类成分,具有多种强大的生物活性。本研究旨在探讨 EGCG 对内质网(ER)应激介导的炎症的影响,并阐明其在 2 型糖尿病肾脏中的潜在分子机制。雄性大鼠随机分为四组:正常组、糖尿病组、低剂量 EGCG 组和高剂量 EGCG 组。在 2 型糖尿病大鼠中,高血糖和高血脂明显导致肾脏结构损伤和功能障碍,并加重 ER 应激。同时,持续的 ER 应激激活 NOD 样受体家族 pyrin 结构域包含 3(NLRP3)炎性小体,从而上调糖尿病肾脏中炎症细胞因子的含量。补充 40mg/kg 和 80mg/kg EGCG 后,明显改善了高血糖、高血脂以及肾脏组织病理学改变和功能障碍;EGCG 治疗组中肾 ER 应激、NLRP3 炎性小体和炎症反应明显受到抑制。综上所述,本研究强调了 EGCG 在 2 型糖尿病中的肾脏保护作用,其机制主要与抑制 ER 应激介导的 NLRP3 炎性小体过度激活有关。