摘要
目的 探讨bcl 2基因在梗阻性黄疸 (梗黄 )大鼠肝细胞损害中的调控作用。方法 采用胶原酶原位肝灌注法获取对照组大鼠肝细胞及梗黄实验组术后 3 ,7,14 ,2 1d大鼠的肝细胞。 (1)分离的对照组及实验组大鼠肝细胞分别用RT PCR检测bcl 2mRNA的表达 ;(2 )分离对照组及实验组14d组大鼠的肝细胞行原代培养后 ,使用 10 0 μM甘氨鹅脱氧胆酸钠 (GCDC )作用于两组肝细胞 2 4h后 ,用FCM法测定肝细胞的凋亡比率 ,用TUNEL技术进行肝细胞凋亡的原位检测。结果 (1)RT PCR检测表明 ,对照组大鼠肝细胞无bcl 2mRNA表达 ,实验组术后 7,14 ,2 1d组大鼠肝细胞均有bcl 2mR NA表达 ;(2 )GCDC作用两组大鼠肝细胞后 ,实验组比对照组肝细胞凋亡明显减少 (P <0 .0 0 1)。结论 (1)阻塞性黄疸大鼠肝细胞有bcl 2基因的表达 ,正常大鼠肝细胞则无此表达 ;(2 )在阻塞性黄疸过程中 ,大鼠肝细胞通过表达bcl 2来抑制胆盐致肝细胞的凋亡作用。
Objective To explore the regulating mechanism of bcl 2 gene in hepatocyte injury caused by obstructive jaundice in rats. Methods Normal rats' and bile duct ligated 7d,14d,21d rats' hepatocytes were isolated by in situ collagenase perfusion and primary culture. (1) bcl 2 mRNA was detected by RT PCR in all cells; (2) After normal rat and bile duct ligated 14d rat hepatocytes were added 100μM GCDC and kept for 24hrs, cells were evaluated by FCM and TUNEL. Results (1) Normal rat hepatocytes did not express bcl 2 by RT PCR technique. bcl 2 was expressed in 7-,14-,21-day BDL rats. (2) After adding 100μM GCDC and keeping for 24hrs, the apoptosis of bile duct ligated rat hepatocytes significantly decreased compared with that of normal rat hepatocytes. Conclusions (1) Bile duct ligated rat hepatocytes expressed bcl 2. (2) Hepatocellular expression of bcl 2 during obstructive jaundice is an adaptive phenomenon to resist apoptosis by bile salts.
出处
《中国普通外科杂志》
CAS
CSCD
2003年第3期202-205,共4页
China Journal of General Surgery
