论文部分内容阅读
我们以往的研究证明,大鼠再生肝具有抗四氯化碳(CCl_4)损伤的能力。本工作进一步研究其机制,首先从部分(68％)肝切除后不同时间的再生肝提取肝刺激因子(rHSS),用~3H胸腺嘧啶核苷测定rHSS的生物活性,结果表明部分切除肝后72 h的rHSS活性较对照组约增加7.7倍。然后将rHSS注射给小鼠,观察其抗CCl_4损伤肝的效应,具体表现如下:rHSS能减少CCl_4中毒小鼠的死亡率和降低CCl_4所增高的血清谷雨转氨酶(ALT)和谷草转氨酶(AST)的水平。离体实验表明rHSS能提高CCl_4染毒的肝细胞的存活率及减少CCl_4染毒的肝细胞内ALT的漏出,上述实验结果表明rHSS可能是再生肝抗CCl_4损伤的一个重要机制。
Our previous studies demonstrated that rat regenerative liver has the ability to resist CCl 4 injury. In this work, we further studied its mechanism by first extracting hepatic stimulating factor (rHSS) from regenerating liver at different time after partial hepatectomy (68%) and measuring the biological activity of rHSS using ~ 3H thymidine. The results showed that after partial hepatectomy h rHSS activity than the control group increased by about 7.7 times. The mice were then injected with rHSS to observe their anti-CCl 4 -induced liver function. The results were as follows: rHSS could reduce the mortality of CCl 4 -induced mice and decrease the levels of serum ALT and AST Level. In vitro experiments showed that rHSS can increase the survival rate of CCl_4-treated hepatocytes and decrease the leakage of ALT in CCl_4-treated hepatocytes. These results suggest that rHSS may be an important mechanism of anti-CCl_4 injury in regenerative liver.