摘要
为研究四氯化碳（ＣＣＩ４）、血吸虫病和肝炎病毒所致的肝细胞死亡的模型， 以大鼠ＣＣＩ４ 肝损伤、兔血吸虫病和人肝炎后肝硬变为研究对象， 分别以形态学、原位末端标记法（ＴＵＮＥＬ法） 和流式细胞术检测肝细胞凋亡， 并以免疫组化法分析凋亡的调控因素。结果表明：血吸虫病肝、ＣＣＩ４ 大鼠肝、人肝炎后肝硬变肝细胞有凋亡和坏死两种死亡模式， 二者形态不同， 但往往同时存在， 凋亡指数或比率分别为（８．７４±２．４０）％ ， （５．７４±２．４１）％ 和（３．０６±０．７９）％ 。免疫组化： 正常肝Ｂｃｌ－２、ｃ－ｍ ｙｃ、ｃ－ｆｏｓ、ＴＧＦ－β、ＴＮＦα、ｉＮＯＳ均为阴性或弱阳性， 肝损伤模型中均呈阳性或强阳性。结果提示： 凋亡和坏死是肝细胞死亡的两种死亡模式， 并同时存在， 肝细胞凋亡受一系列基因和因子的调控。
The modes of hepatic cell death induced by tetrachloride (CCl 4), schistosomiasis and hepatitis virus were investigated. The modes of hepatic cell death in 30 CCl 4 induced hepatic injury wistar rats, 20 rabbits infected with japonica schistosomiasis and 20 patients infected with chronic hepatitis were subjected to study. Hepatic apoptosis was detected by using morphological technique in situ end labeling methods and flow cytometry (FCM). The regulatory factors of apoptosis were analyzed by using immunohistochemical methods. Results showed that two alternative modes (apoptosis and necrosis) with different morphological patterns of hepatic cell death but coexistence were found in schistosomiasis hepatocytes, CCl 4 induced rat hepatocytes and human post hepatitic cirrhosis hepatocytes. Immunohistochemically, Bcl 2, c myc, c fos, TGF β,TNF α, iNOS were positive immunostaining in the normal liver, and positive or stronger positive in the injured liver. It was concluded that apoptosis and necrosis, two modes of hepatic cell death, are coexistent. Hepatic apoptosis might be regulated by a series of genes and factors.
出处
《同济医科大学学报》
CSCD
1999年第4期313-316,共4页
Acta Universitatis Medicinae Tongji
基金
国家自然科学基金
