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Polysaccharides from mycelia ameliorate insulin resistance in type 2 diabetic mice.菌丝体多糖改善 2 型糖尿病小鼠的胰岛素抵抗。
Food Funct. 2020 Nov 18;11(11):9675-9685. doi: 10.1039/d0fo00728e.
2
Polysaccharides from Armillariella tabescens mycelia ameliorate renal damage in type 2 diabetic mice.银耳菌丝体多糖改善 2 型糖尿病小鼠的肾脏损伤。
Int J Biol Macromol. 2020 Nov 1;162:1682-1691. doi: 10.1016/j.ijbiomac.2020.08.006. Epub 2020 Aug 3.
3
Pathophysiologic mechanisms in diabetic kidney disease: A focus on current and future therapeutic targets.糖尿病肾病的病理生理机制:关注当前和未来的治疗靶点。
Diabetes Obes Metab. 2020 Apr;22 Suppl 1:16-31. doi: 10.1111/dom.13969.
4
Hydrogen sulfide mitigates myocardial inflammation by inhibiting nucleotide-binding oligomerization domain-like receptor protein 3 inflammasome activation in diabetic rats.硫化氢通过抑制核苷酸结合寡聚结构域样受体蛋白 3 炎性小体激活减轻糖尿病大鼠心肌炎症。
Exp Biol Med (Maywood). 2020 Feb;245(3):221-230. doi: 10.1177/1535370219899899. Epub 2020 Jan 13.
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Effects of a combined fucoidan and traditional Chinese medicine formula on hyperglycaemia and diabetic nephropathy in a type II diabetes mellitus rat model.褐藻糖胶与中药配方对 2 型糖尿病大鼠模型高血糖及糖尿病肾病的影响。
Int J Biol Macromol. 2020 Mar 15;147:408-419. doi: 10.1016/j.ijbiomac.2019.12.201. Epub 2019 Dec 24.
6
ER stress response mediates diabetic microvascular complications.内质网应激反应介导糖尿病微血管并发症。
Drug Discov Today. 2019 Dec;24(12):2247-2257. doi: 10.1016/j.drudis.2019.08.003. Epub 2019 Aug 17.
7
Multifactorial functions of the inflammasome component NLRP3 in pathogenesis of chronic kidney diseases.炎症小体组分 NLRP3 在慢性肾脏病发病机制中的多效性功能。
Kidney Int. 2019 Jul;96(1):58-66. doi: 10.1016/j.kint.2019.01.014. Epub 2019 Mar 4.
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Sirtuin-1 ameliorates cadmium-induced endoplasmic reticulum stress and pyroptosis through XBP-1s deacetylation in human renal tubular epithelial cells.Sirtuin-1 通过去乙酰化 XBP-1s 减轻镉诱导的人肾小管上皮细胞内质网应激和细胞焦亡。
Arch Toxicol. 2019 Apr;93(4):965-986. doi: 10.1007/s00204-019-02415-8. Epub 2019 Feb 22.
9
Coadministration of epigallocatechin-3-gallate (EGCG) and caffeine in low dose ameliorates obesity and nonalcoholic fatty liver disease in obese rats.表没食子儿茶素没食子酸酯(EGCG)和咖啡因低剂量联合给药可改善肥胖大鼠的肥胖和非酒精性脂肪性肝病。
Phytother Res. 2019 Apr;33(4):1019-1026. doi: 10.1002/ptr.6295. Epub 2019 Feb 11.
10
Recent Advances in the Understanding of the Health Benefits and Molecular Mechanisms Associated with Green Tea Polyphenols.绿茶多酚的健康益处及其分子机制的研究进展。
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没食子酸表没食子儿茶素酯可改善 2 型糖尿病大鼠肾脏内质网应激介导的炎症。

Epigallocatechin-3-gallate ameliorates renal endoplasmic reticulum stress-mediated inflammation in type 2 diabetic rats.

机构信息

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.

出版信息

Exp Biol Med (Maywood). 2022 Aug;247(16):1410-1419. doi: 10.1177/15353702221106479. Epub 2022 Jul 1.

DOI:10.1177/15353702221106479
PMID:35775606
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9493765/
Abstract

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.

摘要

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。