牛磺酸对四氯化碳致肝细胞凋亡影响的研究

EFFECT OF TAURINE ON CARBON TETRACHLORIDE INDUCED HEPATOCELLULAR APOPTOSIS

本文观察了四氯化碳亚慢性染毒（５００ｍｇ／ｋｇ，每周两次，连续五周）后血清ＡＬＴ、肝脏ＧＳＨ、ＭＤＡ及肝脏的形态学变化，同时研究了牛磺酸（ｔａｕ）对ＣＣｌ４肝毒性的干预作用。结果表明：ＣＣｌ４引起了肝脏明显的脂质过氧化（ＬＰＯ）及肝损伤，但ＡＬＴ与ＭＤＡ之间并不完全并行，说明ＬＰＯ并非肝损伤的唯一原因。ＣＣｌ４组肝组织中凋亡小体明显增加，可能是机体对损伤的一种反应。ｔａｕ干预组肝ＬＰＯ减轻，凋亡小体明显减少，表明ｔａｕ对ＣＣｌ４肝毒性有一定干预作用，其机理可能与ｔａｕ的膜保护作用和水、离子调节作用及抗氧化作用等有关。

Rats were administrated with CCl4 with a dose of 500mg/kg body wt, twice a week for 5weeks. Biochemical indicators including ALT in serum,both GSH and MDA in liver were examined.In addition,the apoptotic bodies (ABs)as well as the general morphologic changes of liver were observed. The results showed that CCl4has induced significant hepatocellular lipid peroxidation(LPO)and injury;The number of ABs in CCl4 group was more than that of other groups. In taurine protected groups,hepatocellular injury was relatively slight compared with the CCl4 group,also in these groups the ABs numbers were prominently decresed.The data of this study indieated that increased ABs in CCl4 group might be a response of the body to chemical damage. Taurine can protect hepatocyte partly against the LPO of CCl4 in vivo.