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首页> 外文期刊>World Journal of Gastroenterology >Alanyl-glutamine dipeptide inhibits hepatic ischemia-reperfusion injury in rats.
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Alanyl-glutamine dipeptide inhibits hepatic ischemia-reperfusion injury in rats.

机译：丙氨酰-谷氨酰胺二肽抑制大鼠肝缺血-再灌注损伤。

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AIM: To investigate the protective effect and mechanism of alanyl-glutamine dipeptide (Ala-Gln) against hepatic ischemia-reperfusion injury in rats. METHODS: Rats were divided into group C as normal control Group (n=16) and group G as alanyl-glutamine pretreatment (n=16). Rats were intravenously infused with 0.9% saline solution in group C and Ala-Gln -enriched (2% glutamine) 0.9% saline solution in group G via central venous catheter for three days. Then all rats underwent hepatic warm ischemia for 30 min followed by different periods of reperfusion. Changes in biochemical parameters,the content of glutathione (GSH) and the activity of superoxide dismutase (SOD) in liver tissue, Bcl-2 and Bax protein expression and morphological changes of liver tissue were compared between both groups. RESULTS: One hour after reperfusion, the levels of liver enzymes in group G were significantly lower than those in group C (P<0.05).Twenty-four hours after reperfusion, the levels of liver enzymes in both groups were markedly recovered and the levels of liver enzyme in group G were also significantly lower than those in group C (P<0.01). One and 24 h after reperfusion, GSH content in group G was significantly higher than that in group C (P<0.05). There was no statistical difference in activities of SOD between the two groups.One and 24 h after reperfusion, the positive expression rate of Bcl-2 protein was higher in group G than in group C (P<0.05) and the positive expression rate of Bax protein was lower in group G than in group C (P<0.05). Histological and ultrastructural changes of liver tissue were inhibited in group C compared to group G. CONCLUSION: Our results suggest that Ala-Gln pretreatment provides the rat liver with significant tolerance to warm ischemia-reperfusion injury,which may be mediated partially by enhancing GSH content and regulating the expression of Bcl-2 and Bax proteins in the liver tissue.
机译：目的：探讨丙氨酰谷氨酰胺二肽（Ala-Gln）对大鼠肝脏缺血再灌注损伤的保护作用及其机制。方法：将大鼠分为正常对照组C组（n = 16）和丙氨酸谷氨酰胺预处理组G（n = 16）。通过中央静脉导管为大鼠静脉注射C组的0.9％盐溶液和G组的0.9％富含Ala-Gln的（2％谷氨酰胺）0.9％盐溶液。然后，所有大鼠经历肝温暖缺血30分钟，然后进行不同时期的再灌注。比较两组肝脏生化指标，谷胱甘肽（GSH）含量，超氧化物歧化酶（SOD）活性，Bcl-2和Bax蛋白表达及肝组织形态学变化。结果：再灌注1小时后，G组肝酶水平明显低于C组（P <0.05）;再灌注后24小时，两组肝酶水平均显着恢复，且均高于正常水平（P <0.05）。 G组肝酶水平也显着低于C组（P <0.01）。再灌注后1和24 h，G组GSH含量明显高于C组（P <0.05）。两组SOD活性无统计学差异。再灌注后1和24 h，G组Bcl-2蛋白阳性表达率高于C组（P <0.05），而Bcl-2蛋白阳性表达率高于C组。 G组Bax蛋白低于C组（P <0.05）。结论：Ala-Gln预处理对大鼠肝脏有明显的抵抗缺血再灌注损伤的作用，其作用可能是通过提高GSH含量部分介导的。并调节肝脏组织中Bcl-2和Bax蛋白的表达。

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