摘要
目的观察氧化槐定碱(Oxysophoridin,OSR)对四氯化碳(CCl4)所致小鼠急性肝损伤的干预效应及对TNF-α和COX-2表达的影响。方法雄性ICR小鼠腹腔注射OSR(125、250、500 mg.kg-1)5d,末次给药结束0.5 h后,腹腔注射CCl4(0.5 mg.kg-1)染毒造模,染毒后2h再次腹腔注射相同剂量的OSR。染毒16h后摘眼球取血,分光光度法测定血清中丙氨酸氨基转移酶(ALT)、天门冬氨酸氨基转移酶(AST)、肝组织中诱生型一氧化氮合酶(iNOS)活性;放射免疫分析法测定血清肿瘤坏死因子-α(TNF-α)的含量;免疫组织化学法测定肝组织中环氧合酶-2(COX-2)。结果 OSR各剂量组可不同程度的降低血清ALT、AST、TNF-α含量(P<0.01),减少肝脏组织COX-2蛋白表达(P<0.01),对iNOS的表达无明显影响。结论 OSR对CCl4所致小鼠急性损伤的肝组织具有一定的保护作用,其机制可能与OSR抑制炎性因子的表达有关。
Objective To explore the effects of oxysophoridine（OSR） on TNF-α,COX-2 and iNOS expression in carbon tetrachloride（CCl4） induce liver injury mice.Methods Mice were treated intraperitoneally with 0.5 ml·kg-1 CCl4 and different groups of animals received OSR（125,250,and 500 mg·kg-1）.At the 16th hour after the CCl4 treatment,the level of serum aminotransferases and tumor necrosis factor-α（TNF-α）,hepatic tissue bomogenate level of inducible nitric oxide synthase（iNOS）,and the protein expression of cycloxygenase-2（COX-2） were detected.Results Compared with model group,the level of serum aminotransferases and TNF-α were significantly increased by the CCl4 treatment but significantly suppressed by OSR.The iNOS did not showed significantly disparation at 16th hour after the CCl4 treatment.OSR could attenuate the increase in the protein expression of COX-2.Conclusion These findings suggest that OSR can protect hepatocytes caused by CCl4 and this protection is likely due to the inhibition of the proinflammatory mediators.
出处
《宁夏医科大学学报》
2011年第7期622-624,F0004,共4页
Journal of Ningxia Medical University
基金
宁夏医科大学面上项目(XM200824)
宁夏医科大学大学生创新项目(XS2007
XS200906)
