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作 者:方德宝[1] 余宏铸[1] 许业传[1] 姚佳明[1] 花香[1] 王欢[1]
机构地区:[1]安徽医科大学第一附属医院普通外科,合肥230022
出 处:《安徽医科大学学报》2011年第8期742-746,共5页Acta Universitatis Medicinalis Anhui
摘 要:目的探讨前列腺素E1(PGE1)对梗阻性黄疸大鼠肝细胞凋亡及相关基因Bax/Bcl-2表达的影响。方法雄性SD大鼠72只,随机分为3组:假手术组(CG组);胆总管结扎组(OJ组);胆总管结扎+PGE1给药组(PE组)。术后再分设3、7、10 d 3个时相点随机采集标本,检测血清肝功能水平,观察肝脏病理形态学改变,测定肝细胞凋亡及Bax/Bcl-2表达的情况。结果①与CG组相比,OJ组和PE组的大鼠血清转氨酶和胆红素水平增高,肝细胞凋亡增多,Bax/Bcl-2的表达增强,并随胆总管结扎时间的延长而愈加明显;②与OJ组同时相点相比,PE组大鼠血清转氨酶和胆红素较低,肝脏组织病理学改变较轻,肝细胞凋亡较少,Bax表达水平较低,而Bcl-2表达较高。结论①PGE1一定程度上可以抑制由梗阻性黄疸所致的大鼠肝细胞凋亡;②PGE1可能通过直接或间接下调促凋亡蛋白Bax、上调抗凋亡蛋白Bcl-2表达而减少梗阻性黄疸时大鼠肝细胞凋亡的发生。Objective To explore the effects of prostaglandin E1(PGE1) on hepatocytes apoptosis,and the expressions of Bax and Bcl-2 in rats with obstructive jaundice(OJ).Methods 72 adult male SD rats were randomly divided into three groups: the sham operation group(CG group),the OJ group and the OJ rats which administered PGE1(PE group).The OJ and the PE groups were established by double-ligating bile duct(BDL).PGE1 with tail vein injection was only administered daily in PE group.Three groups of rats were sacrificed on the 3,7 and 10 days of postoperation respectively.The levels of serum total bilirubin(TBil),direct bilirubin(DBil),alanine aminotransferase(ALT) and aspartate aminotransferase(AST) were tested and the histopathology changes were observed;Apoptosis of hepatocytes was tested by TUNEL and accounted apoptosis index(AI),the immunohistochemical technique was used for detecting the Bax and Bcl-2 protein expression.Results ① With the time of BDL extending,the values of serum ALT,AST,TBil and DBil were increased and OJ group and PE group were higher than those of CG group;The Bcl-2 and Bax protein in OJ and PE group increased with cell apoptosis in hepatic tissue.② Compared with OJ group,the injury degree of hepatic function and histopathology of changes in PE group decreased,the Bcl-2 protein in PE group increased evidently,but Bax decreased.Conclusion PGE1 can ease the degree of hepatic functional injury,which may decrease cell apoptosis by up-regulating the expression of Bcl-2 and down-regulating the expression of Bax in hepatic tissue.
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