EGCG对肾缺血再灌注损伤的保护作用及其作用机制的研究

doi:10.13305/j.cnki.jts.2016.02.007

摘要/Abstract

摘要： 探讨了表没食子儿茶素没食子酸酯（EGCG）对大鼠肾缺血再灌注损伤的保护作用及其机制。结果表明,与肾缺血再灌注损伤模型组相比,EGCG组肾功能改善,肾组织病理改变,Wnt3a、β-catenin、p53、p21、MDA、IL-6、IFN-γ和TNF-α表达明显减少,而CAT,GP_X和SOD表达明显增加。说明EGCG预处理减轻肾缺血再灌注损伤与抑制Wnt3a/β-catenin/p53信号通路介导的炎症反应和氧化应激相关。

关键词: 表没食子儿茶素没食子酸酯, 肾缺血再灌注损伤, 炎症, 氧化应激, Wnt/β-catenin

Abstract: The study aims to investigate potential protection and mechanism of epigallocatechin gallate（EGCG） on kidney ischemia reperfusion injury. The results showed that EGCG treatment improved renal dysfuction, pathlogical change of kidney tissues, and reduced the expression of Wnt3a, β-catenin, MDA, IL-6, IFN-γ and TNF-α, but increased the levels of CAT, GP_X and SOD, suggesting that EGCG can protect the kidney from ischemia-reperfusion injury in rats which is associated with suppressing the activation of Wnt/β-catenin/p53 signaling pathway and inhibiting inflammation and oxidative stress.

Key words: EGCG, kidney ischemia reperfusion injury, inflammation, oxidative stress, Wnt/β-catenin

中图分类号:

刘洪国. EGCG对肾缺血再灌注损伤的保护作用及其作用机制的研究[J]. 茶叶科学, 2016, 36(2): 169-174. doi: 10.13305/j.cnki.jts.2016.02.007.

LIU Hongguo. The Investigation of the Protection Effects and Mechanism of EGCG on Kidney Ischemia Reperfusion Injury[J]. Journal of Tea Science, 2016, 36(2): 169-174. doi: 10.13305/j.cnki.jts.2016.02.007.

参考文献

[1] Shen H, Kreisel D, Goldstein DR.Processes of sterile inflammation[J]. Journal of immunology, 2013, 191(6): 2857-2863.
[2] Kalyanaraman B.Teaching the basics of redox biology to medical and graduate students: Oxidants, antioxidants and disease mechanisms[J]. Redox biology, 2013, 1(1): 244-257.
[3] Kusch A, Hoff U, Bubalo G, et al.Novel signalling mechanisms and targets in renal ischaemia and reperfusion injury[J]. Acta Physiol, 2013, 208(1): 25-40.
[4] Wang Y, He J, Pei X, et al.Systematic review and meta-analysis of mesenchymal stem/stromal cells therapy for impaired renal function in small animal models[J]. Nephrology, 2013, 18(3): 201-208.
[5] Pae M, Wu D.Immunomodulating effects of epigallocatechin-3-gallate from green tea: mechanisms and applications[J]. Food & Function, 2013, 4(9): 1287-1303.
[6] Camfield DA, Stough C, Farrimond J, et al.Acute effects of tea constituents L-theanine, caffeine, and epigallocatechin gallate on cognitive function and mood: a systematic review and meta-analysis[J]. Nutr Rev, 2014, 72(8): 507-522.
[7] Lv J, Feng M, Zhang L, et al.Protective effect of epigallocatechin gallate, a major constituent of green tea, against renalischemia-reperfusion injury in rats[J]. Int Urol Nephrol, 2015, 47(8): 1429-1435.
[8] Legeay S, Rodier M, Fillon L, et al.Epigallocatechin gallate: a review of its beneficial properties to prevent metabolic syndrome[J]. Nutrients, 2015, 7(7): 5443-5468.
[9] Takizawa Y, Kitazato T, Kishimoto H, et al.Effects of antioxidants on drug absorption in in vivo intestinal ischemia/reperfusion[J]. Eur J Drug Metab Pharmacokinet, 2011, 35(3/4): 89-95.
[10] Zhang F, Li N, Jiang L, et al.Neuroprotective Effects of (-)-epigallocatechin-3-gallate against focal cerebralischemia/reperfusion injury in rats through attenuation of inflammation[J]. Neurochem Res, 2015, 40(8): 1691-1698.
[11] Lee SK, Kim JH, Kim JS, et al.Polyphenol (-)-epigallocatechin gallate-induced cardioprotection may attenuate ischemia-reperfusion injury through adenosine receptor activation: a preliminary study[J]. Korean J Anesthesiol, 2012, 63(4): 340-345.
[12] Vaseva AV, Moll UM.The mitochondrial p53 pathway[J]. Biochim Biophys Acta, 2009, 1787(5): 414-420.
[13] Miura T, Nishihara M, Miki T.Drug development targeting the glycogen synthase kinase-3beta (GSK-3beta)-mediated signal transduction pathway: role of GSK-3beta in myocardial protection against ischemia/reperfusion injury[J]. J Pharmacol Sci, 2009, 109(2): 162-167.
[14] Xia Y, He Z, Liu B, et al.Downregulation of Meg3 enhances cisplatin resistance of lung cancer cells through activation of the Wnt/β-catenin signaling pathway[J]. Mol Med Rep, 2015, 12(3): 4530-4537.
[15] Szlachcic WJ, Switonski PM, Krzyzosiak WJ, et al.Huntington disease iPSCs show early molecular changes in intracellular signaling, the expression of oxidative stress proteins and the p53 pathway[J]. Dis Model Mech, 2015, 8(9): 1047-1057.