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本文旨在研究亚硝酸钠预处理对急性酒精损伤小鼠肝脏的保护作用。将40只C57bL/6 小鼠随机分为4组:急性酒精肝损伤组腹腔注射乙醇(4.5 g/kg);亚硝酸钠预处理组腹腔注射亚硝酸钠(16 mg/kg) 12 h后,再给予乙醇(4.5 g/kg);对照组仅给予生理盐水;单纯亚硝酸钠组仅给予亚硝酸钠(16 mg/kg)。处理结束时检测肝脏指数,比色法检测肝组织超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GSH-Px)、过氧化氢酶(CAT)活性,丙二醛(MDA)含量及血清丙氨酸转氨酶(ALT)和天门冬氨酸转氨酶(AST)活性,HE和荧光标记TUNEL染色观察肝组织病理学改变,免疫组织化学染色法和Western blot检测缺氧诱导因子-1α (HIF-1α)蛋白表达。结果显示,与急性酒精肝损伤组相比,亚硝酸钠预处理组肝脏指数、血清ALT和AST活性显著下降,急性酒精损伤引起的小鼠肝组织病理学变化得到改善,坏死程度明显减轻,肝组织SOD、GSH-Px、CAT活性增加,MDA含量和细胞凋亡指数降低,肝细胞内HIF-1α蛋白表达水平显著升高。以上结果提示,亚硝酸钠预处理可减轻急性酒精肝损伤,其机制涉及氧化应激的抑制和HIF-1α蛋白水平的上调。
This article aims to study the protective effects of sodium nitrite preconditioning on the liver of mice with acute alcohol injury. Forty C57BL / 6 mice were randomly divided into four groups: alcohol (4.5 g / kg) was given intraperitoneally to alcoholic liver injury group, sodium nitrite (16 mg / kg) Ethanol (4.5 g / kg) was given again; the control group was given saline only; sodium nitrite alone was given only sodium nitrite (16 mg / kg). The liver index was measured at the end of treatment, and the activities of superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), catalase (CAT), malondialdehyde ) And serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST) activity were detected by HE staining and fluorescent labeled TUNEL staining. Immunohistochemical staining and Western blot were used to detect the expression of hypoxia inducible factor-1α (HIF-1α) protein expression. The results showed that compared with acute alcoholic liver injury group, the liver index, serum ALT and AST activity of sodium nitrite pretreatment group decreased significantly, the pathological changes of liver tissue induced by acute alcohol injury were improved, the degree of necrosis was significantly reduced, The activities of SOD, GSH-Px, CAT increased, MDA content and apoptosis index decreased, and the expression of HIF-1α protein in hepatocytes increased significantly. The above results suggest that sodium nitrite pretreatment can reduce acute alcoholic liver injury, its mechanism involves the inhibition of oxidative stress and HIF-1α protein levels.