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目的研究低剂量内毒素(LPS)预处理对LPS介导的小鼠急性肝损伤的影响。方法LPS通过腹腔注射小鼠;丁基亚磺酰亚胺(BSO)处理耗尽小鼠肝脏谷胱苷肽(GSH)含量;血浆天冬氨酸氨基转移酶(AST)和丙氨酸氨基转移酶(ALT)测定用全自动生化分析仪;基因表达测定采用RT-PCR。结果①低剂量LPS预处理降低高剂量LPS诱导的小鼠肝功能损伤;②低剂量LPS刺激肝脏GSH含量升高;LPS预处理组GSH水平显著高于高剂量LPS处理组;③BSO预处理后,LPS预处理组与高剂量LPS组的血浆ALT和AST水平没有差别;④LPS处理导致转硫途径关键酶——胱硫醚β合酶活性以及GSH合成途径关键酶——γ-谷氨酰半胱氨酸合成酶表达升高。结论低剂量LPS通过上调肝组织中GSH合成相关基因表达,增加GSH的含量,减轻高剂量LPS诱导的肝脏损伤。
Objective To investigate the effect of low dose lipopolysaccharide (LPS) pretreatment on LPS-induced acute liver injury in mice. Methods LPS was intraperitoneally injected into mice. Butyl sulfoximine (BSO) was used to deplete glutathione (GSH) in liver of mice. Plasma aspartate aminotransferase (AST) and alanine aminotransferase Enzyme (ALT) determination with automatic biochemical analyzer; gene expression was determined by RT-PCR. Results ① Low-dose LPS pretreatment reduced high-dose LPS-induced liver injury in mice; ② Low dose LPS stimulated hepatic GSH levels increased; LPS pretreatment group GSH levels were significantly higher than the high dose LPS treatment group; ③ BSO pretreatment, LPS pretreatment group and high dose LPS group plasma ALT and AST levels there is no difference; ④ LPS treatment led to the key enzyme in the sulfur transfer pathway - cystathionine β-synthase activity and GSH synthesis pathway key enzyme - γ-glutamylcysteine Increased expression of the protein synthase. Conclusion Low-dose LPS can up-regulate the expression of GSH-related genes in liver tissue, increase the content of GSH and relieve the liver damage induced by high dose LPS.