藏茵陈对小鼠冠状病毒性肝炎细胞caspase-3影响  

Effect of Tibetan Artemisiae Capillaries on caspase-3 in mice with hepatitis virus infection

作　　者：苏丽贤[1] 汤朝晖[1] 罗炳徳 林培政[2] 万为人[1] 郭进强[1] 

机构地区：[1]南方医科大学公共卫生与热带医学学院儿少卫生学系,广东广州510515 [2]广州中医药大学

出　　处：《中国公共卫生》2012年第1期56-58,共3页Chinese Journal of Public Health

基　　金：国家自然科学基金-广东省联合基金(U0632009)

摘　　要：目的观察小鼠冠状病毒性肝炎肝细胞中caspase-3介导的凋亡机制变化,探讨藏茵陈对其干预作用及相关机制。方法将24只小鼠随机分成对照组、模型组、阳性对照组和藏茵陈组,造模成功后用赖氏法测定小鼠血清肝功能2项,苏木素-伊红染色光镜观察小鼠肝脏病理变化,用酶标仪检测肝匀浆caspase-3活性,用荧光定量PCR检测肝组织中Fas和caspase-3 mRNA含量。结果与对照组比较,模型组小鼠ALT、AST活力分别为(225.349±9.904)、(180.823±17.34)U/L,明显升高;病理切片显示肝脏损伤明显,caspase-3活性(0.371±0.051)、Fas和caspase-3 mRNA含量(1.93±0.08、0.867±0.102)均明显升高;藏茵陈干预后ALT、AST分别为(181.906±20.164)和(139.824±12.153)U/L,Fas和caspase-3 mRNA含量为(1.673±0.047)和(0.518±0.103),明显低于模型组(P<0.05),病理切片显示,藏茵陈组小鼠肝脏损伤与模型组比较有所改善。结论 Fas诱导的caspase-3细胞凋亡可能是小鼠冠状病毒性肝炎的致病机制之一,藏茵陈可通过抑制细胞凋亡并改善肝脏损伤程度。Objective To observe the changes of caspase-3 in liver cells of mice with hepatitis virus infection, and to explore the intervening effect and mechanism of Tibetan Artemisiae Capillaries （TAC） on caspase-3. Methods Twenty- four mice were randomly divided into four groups：control group, model group, virazole group, and TAC group. Then serum contents of alanine aminotransferase（ALT） and asparate aminotransferase（AST） were detected with Lai＇s method and path- ological changes of the liver were observed with light microscope after haematoxylin eosin （HE） staining. The activity of caspase-3 was detected by microplate reader. The contents of factor associated suicide （Fas） and caspase-3 mRNA were detected by quantitative PCR. Results Compared with the control group, all of the indicators of the model group increased. The content of ALT was 225. 349 ± 9. 904 and that of AST was 180. 823 ± 17. 34. The activity of caspase-3 was 0. 371 ± 0. 051. The contents of Fas and caspase-3 mRNA were 1.93 ± 0. 08 and 0. 867 ± 0. 102. The pathological observation revealed obvious damage of the liver. After the treatment of TAC, the contents of ALT（ 181. 906 ± 20. 164 ）, AST （ 139. 824 ± 12. 153） ,Fas（ 1. 673±0. 047） ,and caspase-3 mRNA（0. 518 ±0. 103） showed obvious decrease,and the same as the activity of caspase-3 （0. 202 ± 0. 029）. The pathologic damage of the TAC group was alleviated compared with that of the model one. Conclusion The apoptosis induced by Fas/FasL may be one of the mechanism of the hepatitis caused by mouse hepatitis virus-A59 （ MHV-A59 ）. Tibetan Artemisiae Capillaries can suppress the apoptosis and weaken the damage of the liver.

关 键 词：藏茵陈 鼠肝炎冠状病毒 FAS CASPASE-3 

分 类 号：R512.6[医药卫生—内科学]