促红细胞生成素预处理通过抗凋亡减轻肠缺血再灌注损伤

促红细胞生成素预处理通过抗凋亡减轻肠缺血再灌注损伤刘启胜;程正位;熊建光;程思;李湘楚
【期刊名称】《实用药物与临床》
【年(卷),期】2015(018)010
【摘要】目的探讨促红细胞生成素( Erythropoietin,EPO)预处理对大鼠肠缺血再灌注损伤的作用及机制. 方法 24只雄性SD大鼠随机分为3组:假手术组( Sham 组)、肠缺血再灌注损伤组( IRI组)、促红细胞生成素预处理组(EPO组),每组8只. Sham组、IRI组手术前1 h给予生理盐水(5 000 U/kg,腹腔注射),EPO组缺血前1 h给予促红细胞生成素(5 000 U/kg,腹腔注射),IRI组和EPO组采用血管夹夹闭肠系膜上动脉,置于32 ℃温箱后45 min后松开血管夹. Sham组操作同上,但不夹闭肠系膜上动脉. 再灌注1 h后处死大鼠,收集血清和小肠标本. HE 染色后观察小肠病理学形态学变化,采用 Western blot 检测 EPOR、p-EPOR、JAK2、p-JAK2、p-STAT3、STAT3、Bax、Cleavage-caspase3、Bcl-2、Caspase3. 结果与 Sham 组比较,IRI 组病理改变及 p-EPOR、p-JAK2、p-STAT3、Bax、Cleavage-caspase3表达明显增加( P <0. 05 ),Bcl-2、Caspase3 表达减少( P <0. 05 ). 与IRI组比较,EPO组病理改变、Cleavage-caspase3蛋白表达减少(P<0. 05),p-EPOR、p-JAK2、p-STAT3、Bcl-2、Caspase3表达明显增加(P<0. 05). 结论促红细胞生成素预处理可通过诱导JAK2/STAT3 信号通路激活而抑制凋亡,减轻肠缺血再灌注损伤.%Objective To discuss the effect and potential mechanism of EPO on intestinal ischemia reperfusion injury. Methods 24 male SD rats were randomly allocated into 3 groups: Sham operation group ( Sham group,n=8),intestinal ischemia reperfusion injury group (IRI
group,n=8),and EPO pretreatment group (EPO group,n=8). Rats in IRI group and Sham group were pretreated with saline (5 000 U/kg,i. p. ) at 1 h before operation,while rats in EPO group received EPO (5 000 U/kg,i. p. ). Rats in IRI group and EPO group were kept in 32 ℃ infant incubators for 45 min after clamping the superior mesenteric artery ( SMA),then the clamp was removed for reperfusion. Rats in sham group underwent the same process,except for clamping SMA. The rats were sacrificed after 1 h of reperfu-sion. Blood samples and intestinal tissues were collected. The pathology of intestinal tissues was observed according to HE staining,the protein levels of EPOR,p-EPOR,JAK2,p-JAK2,p-STAT3,STAT3,Bax,Cleavage-caspase3,Bcl-2 and Caspase3 were measured by Western blot. Results Compared with sham group,the intestinal histology change,the protein expression level of p-EPOR p-JAK2,p-STAT3,Bax and Cleavage-caspase3 in IRI group increased significantly (P<0. 05),while the expression of Bcl-2 and Caspase3 decreased (P<0. 05). Compared with IRI group,the intestinal histology change,the protein expression level of Cleavage-caspase3 in EPO group decreased significantly (P<0. 05),while the p-EPOR p-JAK2,p-
STAT3,Bcl-2 and Caspase3 increased (P<0. 05). Conclusion EPO pretreatment could inhibit the apoptosis to improve the intestinal ischemia reperfusion injury by inducing the activation of JAK2/STAT3 signal pathway.【总页数】4页(P1154-1157)
【作者】刘启胜;程正位;熊建光;程思;李湘楚
【作者单位】咸宁市中心医院消化内科,咸宁437100;咸宁市中心医院消化内科,咸宁437100;咸宁市中心医院消化内科,咸宁437100;咸宁市中心医院消化内科,咸宁437100;咸宁市中心医院消化内科,咸宁437100
【正文语种】中文
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