摘要
目的 :探讨丹参对大鼠肝脏缺血再灌注时肝细胞凋亡及相关基因 (Bcl-2和 Bax)表达的作用。方法 :SD大鼠随机分为假手术 (SO)组、缺血再灌注 (IP)组及丹参 (SM)治疗组 ,并根据再灌注不同时间点再分为 7个亚组。后 2组缺血时间均为 30 min。分别于再灌注 0、1、6、12、2 4、48、72 h后采取肝脏组织标本。分别采用原位末端标记 (TU NEL)技术和免疫组化 ,检测大鼠肝组织细胞凋亡及 Bcl-2、Bax蛋白表达水平。结果 :缺血再灌注组细胞凋亡 1h开始出现 ,12～ 2 4h达峰值 ,Bcl-2、Bax的表达增强 ;2 4h后凋亡峰缓慢下降 ,Bcl-2、Bax的表达陆续减弱。丹参治疗组与缺血再灌注组相比于 1～ 72 h各时间点 Bcl-2表达增强 ,Bax表达减弱 ,凋亡细胞数明显减少 (P<0 .0 5 ,P<0 .0 1)。结论 :丹参可通过增强 Bcl-2表达 ,抑制 Bax表达 ,而抑制肝脏缺血再灌注时肝细胞凋亡。因而可以预防肝脏缺血再灌注损伤。
Objective:To study the effect of salvia miltiorrhiza (SM) on the hepatocytes apoptosis and expression of its relative gene(Bcl-2,Bax) in rat liver following hepatic ischemia-reperfusion.Methods:SD rats was randomly divided into sham-operation (SO) group, ischemia-reperfusion(IP)group and salvia miltiorrhiza (SM)group.The three groups were divided into 7subgroups respectively .The latter two groups were subjected to 30 minutes’ of ischemia.The liver specimen were collected after reperfusion for 0、1、6、12、24、48、72 hours respectively,then hepatocytes apoptosis andBcl-2 and Bax gene expression of liver tissue were studied respectively by in situ terminal deoxynucleotidyl transferase mediated dUTP-FITC nick end-labeling (TUNEL) technique and immunohistochemistry.Results:In the IP group,apoptotic phenomenon was found at 1h,the index of apoptosis was significantly increased at 12-24h after reperfusion,the expression of Bcl-2、Bax was increased correspondingly; The index of apoptosis and the expression of Bcl-2、Bax were decreased after 24h by inches. The expression of Bcl-2 gene elevated and expression of Bax gene and cell apoptosis decreased in salvia miltiorrhiza treated rats compared with ischemia-reperfusion rats (P<0.05,P<0.01).Conclusion:Salvia miltiorrhiza can increase Bcl-2 expression, decrease Bax expression and inhibit hepatocytes apoptosis. SM may play a positive role in preventing hepatic ischemia-reperfusion injury.
出处
《南通医学院学报》
2003年第4期410-411,413,共3页
ACTA Academiae Medicinae Nantong
关键词
细胞凋亡
丹参
基因表达
肝脏缺血再灌注
大鼠
Apoptosis
Salvia Miltiorrhiza
Gene expression
Hepatic ischemia-reperfusion
Rat
