实用药物与临床
實用藥物與臨床
실용약물여림상
Practical Pharmacy and Clinical Remedies
2015年
10期
1154-1157
,共4页
刘启胜%程正位%熊建光%程思%李湘楚
劉啟勝%程正位%熊建光%程思%李湘楚
류계성%정정위%웅건광%정사%리상초
促红细胞生成素%肠缺血再灌注损伤%凋亡%JAK2/STAT3
促紅細胞生成素%腸缺血再灌註損傷%凋亡%JAK2/STAT3
촉홍세포생성소%장결혈재관주손상%조망%JAK2/STAT3
Erythropoietin%Intestinal ischemia reperfusion injury%Apoptosis%JAK2/STAT3
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.
目的 探討促紅細胞生成素( Erythropoietin,EPO)預處理對大鼠腸缺血再灌註損傷的作用及機製. 方法 24隻雄性SD大鼠隨機分為3組:假手術組( Sham組)、腸缺血再灌註損傷組( IRI組)、促紅細胞生成素預處理組(EPO組),每組8隻. Sham組、IRI組手術前1 h給予生理鹽水(5 000 U/kg,腹腔註射),EPO組缺血前1 h給予促紅細胞生成素(5 000 U/kg,腹腔註射),IRI組和EPO組採用血管夾夾閉腸繫膜上動脈,置于32 ℃溫箱後45 min後鬆開血管夾. Sham組操作同上,但不夾閉腸繫膜上動脈. 再灌註1 h後處死大鼠,收集血清和小腸標本. HE 染色後觀察小腸病理學形態學變化,採用 Western blot 檢測 EPOR、p-EPOR、JAK2、p-JAK2、p-STAT3、STAT3、Bax、Cleavage-caspase3、Bcl-2、Caspase3. 結果 與 Sham 組比較,IRI 組病理改變及 p-EPOR、p-JAK2、p-STAT3、Bax、Cleavage-caspase3錶達明顯增加( P <0. 05 ),Bcl-2、Caspase3 錶達減少( P <0. 05 ). 與 IRI組比較,EPO組病理改變、Cleavage-caspase3蛋白錶達減少(P<0. 05),p-EPOR、p-JAK2、p-STAT3、Bcl-2、Caspase3錶達明顯增加(P<0. 05). 結論 促紅細胞生成素預處理可通過誘導JAK2/STAT3 信號通路激活而抑製凋亡,減輕腸缺血再灌註損傷.
목적 탐토촉홍세포생성소( Erythropoietin,EPO)예처리대대서장결혈재관주손상적작용급궤제. 방법 24지웅성SD대서수궤분위3조:가수술조( Sham조)、장결혈재관주손상조( IRI조)、촉홍세포생성소예처리조(EPO조),매조8지. Sham조、IRI조수술전1 h급여생리염수(5 000 U/kg,복강주사),EPO조결혈전1 h급여촉홍세포생성소(5 000 U/kg,복강주사),IRI조화EPO조채용혈관협협폐장계막상동맥,치우32 ℃온상후45 min후송개혈관협. Sham조조작동상,단불협폐장계막상동맥. 재관주1 h후처사대서,수집혈청화소장표본. HE 염색후관찰소장병이학형태학변화,채용 Western blot 검측 EPOR、p-EPOR、JAK2、p-JAK2、p-STAT3、STAT3、Bax、Cleavage-caspase3、Bcl-2、Caspase3. 결과 여 Sham 조비교,IRI 조병리개변급 p-EPOR、p-JAK2、p-STAT3、Bax、Cleavage-caspase3표체명현증가( P <0. 05 ),Bcl-2、Caspase3 표체감소( P <0. 05 ). 여 IRI조비교,EPO조병리개변、Cleavage-caspase3단백표체감소(P<0. 05),p-EPOR、p-JAK2、p-STAT3、Bcl-2、Caspase3표체명현증가(P<0. 05). 결론 촉홍세포생성소예처리가통과유도JAK2/STAT3 신호통로격활이억제조망,감경장결혈재관주손상.
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.
