EGCG对小鼠肝缺血再灌注损伤的保护作用

发布时间：2018-06-11 10:16

本文选题：表没食子儿茶素没食子酸酯 + 缺血再灌注　；参考：《现代免疫学》2015年03期

【摘要】：本研究旨在探讨表没食子儿茶素没食子酸酯[(-)-Epigallocatechin-3-gallate,EGCG]对BALB/c小鼠肝缺血再灌注损伤的保护作用。取健康雄性Balb/c小鼠18只,随机分3组(n=6),分别为:对照组(Sham组)、缺血再灌注组(I/R组)和I/R+EGCG处理组(EGCG组)。各组分别于再灌注末摘除眼球取血样,处死小鼠收集肝组织。测定血清中谷丙转氨酶(ALT)、谷草转氨酶(AST)水平;取缺血再灌注肝叶(左外叶肝)组织行HE染色后光镜下观察其病理形态学改变;免疫组织化学测定TLR4(Toll-like receptor4,TLR4)和NF-κB P65(nuclear transcription fator-kappa B P65)蛋白的表达量。结果发现,经EGCG预处理后,EGCG组小鼠血清AST、ALT的水平明显低于IR组(P0.05),而显著高于Sham组(P0.01)。HE染色结果显示,EGCG组左外叶肝组织损伤程度明显小于IR组,但较Sham组显著增大。免疫组化结果显示,EGCG组TLR4及NF-κB P65蛋白的阳性表达评分分别为(6.67±1.97分,5.67±1.51分)比I/R组(9.00±1.55分,8.33±2.25分)明显降低(P0.05),较Sham组(3.00±0.98分,2.83±0.98分)显著升高(P0.01)。设对照组基准值为1.00,real time-PCR结果示,I/R组左外叶肝组织中IL-1b和TNF-α的mRNA相对表达水平较EGCG组明显增高(P0.05),同时EGCG组较Sham组显著增高(P0.01)。研究表明,EGCG可抑制炎症反应,减少肝组织缺血再灌注损伤,其机制可能与EGCG调节TLR4/NF-κB P65信号通路及通路下游TNF-α、IL-6等炎症分子表达的变化有关。
[Abstract]:The aim of this study was to investigate the protective effect of epigallocatechin-3-gallate EGCG on hepatic ischemia-reperfusion injury in BALB / c mice. Eighteen healthy male Balb / c mice were randomly divided into 3 groups: control group (Sham group), ischemia reperfusion group (I / R group) and I / R EGCG treatment group (EGCG group). Blood samples were removed from eyeballs at the end of reperfusion and liver tissues were collected. The serum levels of alanine aminotransferase (alt) and glutamic oxaloacetic transaminase (AST) were measured, and the histopathological changes of hepatic lobe (left lateral lobe) were observed under light microscope after HE staining. The expression of TLR4Toll-like receptor4 (TLR4) and NF- 魏 B P65nuclear transcription fator-kappa B (P65) protein were detected by immunohistochemistry. The results showed that the level of serum alt in EGCG group was significantly lower than that in IR group, but significantly higher than that in Sham group. The results showed that the damage degree of left lateral lobe liver in EGCG group was significantly lower than that in IR group, but it was significantly higher than that in Sham group. Immunohistochemical results showed that the expression of TLR4 and NF- 魏 B p65 protein in EGCG group was 6.67 卤1.97 and 5.67 卤1.51 respectively, which was significantly lower than that in I / R group (9.00 卤1.55, 8.33 卤2.25), and significantly higher than that in Sham group (3.00 卤0.98, 2.83 卤0.98). Compared with EGCG group, the relative expression of IL-1b and TNF- 伪 mRNA in the left lateral lobe liver in the control group was significantly higher than that in the EGCG group, and the expression of IL-1b and TNF- 伪 mRNA in the left lateral lobe liver tissue in the EGCG group was significantly higher than that in the Sham group, while the expression of IL-1b and TNF- 伪 mRNA in the left lateral lobe liver in the EGCG group was significantly higher than that in the Sham group. It is suggested that EGCG can inhibit inflammatory response and decrease hepatic ischemia-reperfusion injury. The mechanism of EGCG may be related to the regulation of TLR4 / NF- 魏 B p65 signaling pathway and its downstream TNF- 伪 IL-6 expression.
【作者单位】：广西医科大学附属肿瘤医院;
【基金】：广西医科大学青年科学基金(02602211011) 广西自然科学青年基金(2013GXNSFBA019186) 广西科学研究与技术开发计划(1298003-2-9)
【分类号】：R392

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