Protective effects of epigallocatechin-3-gallate on intestinal ischemia reperfusion injury through enhanced activation of PI3K/Akt pathway in rats
Protective effects of epigallocatechin-3-gallate on intestinal ischemia reperfusion injury through enhanced activation of PI3K/Akt pathway in rats
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表没食子儿茶素-3-没食子酸酯通过增强 PI3K/Akt 通路激活对大鼠肠缺血再灌注损伤的保护作用
DOI：
10.1007/s11596-015-1441-2
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发表时间：
2015-06
影响因子：
--
通讯作者：
Chen Zhi-shui
中科院分区：
文献类型：
--
作者：
Zhang Xuan;He Fan;Yang Jun;Chen Zhi-shui
炎症在肠缺血再灌注损伤（IRI）中起关键作用。表没食子儿茶素-3-没食子酸酯（EGCG）已被证明具有抗炎作用。本研究探讨了EGCG对肠道IRI的影响及其可能的作用机制。雄性Wistar大鼠随机分为假手术组（Sham）、IRI对照组（IRI）和IRI-EGCG组（EGCG）。IRI-EGCG组大鼠在IRI诱导前给予溶解于饮用水中的EGCG（0.4mg/mL）14天。结扎上级肠系膜动脉（SMA）30 min，再灌注1 h，建立大鼠肠道IRI模型。检查肠组织学、促炎细胞因子和介质，并评估EGCG对PI 3 K/Akt信号传导的影响。EGCG能显著减轻肠组织病理改变，抑制IR诱导的血清和肠组织TNF-α、IL-1和IL-6 mRNA和蛋白表达的上调。其机制可能与EGCG增强了PI 3 K/Akt信号通路的激活有关。结论：EGCG可通过激活PI 3 K/Akt信号通路抑制炎症反应，从而显著减轻大鼠急性肠道IRI，有望成为临床上预防或治疗肠道IRI的一种新方法。
Inflammation plays a critical role in intestinal ischemia reperfusion injury (IRI). Epigallocatechin-3-gallate (EGCG) has been demonstrated to possess anti-inflammatory effect. This study examined the effect of EGCG on intestinal IRI and explored the possible mechanisms. Male Wistar rats were randomly divided into three groups: sham-operated group (Sham), IRI control group (IRI) and IRI-EGCG group (EGCG). Rats in IRI-EGCG group were administered dissolved EGCG in drinking water (0.4 mg/mL) for 14 days prior to IRI induction. A rat model of intestinal IRI was established by ligating the superior mesenteric artery (SMA) for 30 min, followed by reperfusion for 1 h. Intestinal histology, pro-inflammatory cytokines and mediators were examined and the effect of EGCG on PI3K/Akt signalling was assessed. EGCG significantly alleviated the pathological changes of the intestine and suppressed the IRI-induced up-regulation of TNF-α, IL-1 and IL-6 mRNA and protein expression in the serum and intestine. The mechanism might be that EGCG enhanced the activation of PI3K/Akt signalling pathway. In conclusion, the administration of EGCG can significantly mitigate the acute intestinal IRI in rats by enhancing the activation of PI3K/Akt signalling pathway to suppress inflammatory response and might be a promising alternative for the prevention or treatment of intestinal IRI in the clinical practice.
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影响因子：
3.2
作者：
M. Fink
通讯作者：
M. Fink
影响因子：
5.4
作者：
Bagchi, Parikshit;Nandi, Satabdi;Chawla-Sarkar, Mamta
通讯作者：
Chawla-Sarkar, Mamta
影响因子：
6.1
作者：
Chen Shi-da;Chen Ya-bin;Tan Zhi
通讯作者：
Tan Zhi
DOI：
10.3233/jad-140981
发表时间：
2015
期刊：
Journal of Alzheimer's disease : JAD
影响因子：
--
作者：
Jennifer M. Walker;Diana Klakotskaia;Deepa Ajit;G. Weisman;W. Wood;G. Sun;P. Serfozo;Á. Simonyi-Á.-Simon
通讯作者：
Jennifer M. Walker;Diana Klakotskaia;Deepa Ajit;G. Weisman;W. Wood;G. Sun;P. Serfozo;Á. Simonyi-Á.-Simon
DOI：
10.1016/j.bbrc.2012.03.013
发表时间：
2012-04-06
影响因子：
3.1
作者：
Al-Maghrebi, May;Renno, Waleed M.;Al-Ajmi, Nada
通讯作者：
Al-Ajmi, Nada