中华急诊医学杂志
中華急診醫學雜誌
중화급진의학잡지
Chinese Journal of Emergency Medicine
2015年
10期
1131-1134
,共4页
王艳华%苏文利%郝平%朱文献%邵伟怡%钱龙杰%王毅鑫
王豔華%囌文利%郝平%硃文獻%邵偉怡%錢龍傑%王毅鑫
왕염화%소문리%학평%주문헌%소위이%전룡걸%왕의흠
p55TNFR%缺血-再灌注%心脏损伤%氧化应激
p55TNFR%缺血-再灌註%心髒損傷%氧化應激
p55TNFR%결혈-재관주%심장손상%양화응격
p55TNFR%Ischemia-reperfusion%Myocardial injury%Oxidative stress
目的 研究p55TNFR选择性淋巴毒素对缺血-再灌注后心脏损伤的保护作用,并探讨其作用机制.方法 SD大鼠40只随机(随机数字法)分为4组,A组为假手术组,B组为大鼠心脏缺血-再灌注(I/R)模型组,C组为25 μg/(kg·d)野生型淋巴毒素(rhLTα)治疗组,D组为25 μg/ (kg·d)p55TNFR选择性淋巴毒素(rhLTα-Q107E)治疗组.各组在制备I/R模型后微量泵持续24h静脉滴注生理盐水或治疗药物,24h后检测血浆中心肌酶谱(AST、LDH、CK)、氧化/抗氧化指标(SOD、MDA、GSH-Px),硝基蓝四唑染色计算心肌梗死面积.结果 大鼠心脏缺血-再灌注(I/R)模型心肌梗死面积显著增高,心肌酶谱指标、MDA较假手术组明显升高(P<0.05),SOD和GSH-Px则明显降低(P<0.05).rhLTα-Q107E治疗组可逆转心肌缺血-再灌注后心肌酶谱指标、MDA的升高及SOD和GSH-Px的下降(P<0.05),而野生型rhLTα治疗组的作用不明显(P>0.05).结论 p5STNFR选择性淋巴毒素对大鼠心脏缺血-再灌注后的急性心脏损伤具有保护作用,其机制可能通过直接清除氧自由基、增加内源性抗氧化酶系统的活力而发挥保护作用.
目的 研究p55TNFR選擇性淋巴毒素對缺血-再灌註後心髒損傷的保護作用,併探討其作用機製.方法 SD大鼠40隻隨機(隨機數字法)分為4組,A組為假手術組,B組為大鼠心髒缺血-再灌註(I/R)模型組,C組為25 μg/(kg·d)野生型淋巴毒素(rhLTα)治療組,D組為25 μg/ (kg·d)p55TNFR選擇性淋巴毒素(rhLTα-Q107E)治療組.各組在製備I/R模型後微量泵持續24h靜脈滴註生理鹽水或治療藥物,24h後檢測血漿中心肌酶譜(AST、LDH、CK)、氧化/抗氧化指標(SOD、MDA、GSH-Px),硝基藍四唑染色計算心肌梗死麵積.結果 大鼠心髒缺血-再灌註(I/R)模型心肌梗死麵積顯著增高,心肌酶譜指標、MDA較假手術組明顯升高(P<0.05),SOD和GSH-Px則明顯降低(P<0.05).rhLTα-Q107E治療組可逆轉心肌缺血-再灌註後心肌酶譜指標、MDA的升高及SOD和GSH-Px的下降(P<0.05),而野生型rhLTα治療組的作用不明顯(P>0.05).結論 p5STNFR選擇性淋巴毒素對大鼠心髒缺血-再灌註後的急性心髒損傷具有保護作用,其機製可能通過直接清除氧自由基、增加內源性抗氧化酶繫統的活力而髮揮保護作用.
목적 연구p55TNFR선택성림파독소대결혈-재관주후심장손상적보호작용,병탐토기작용궤제.방법 SD대서40지수궤(수궤수자법)분위4조,A조위가수술조,B조위대서심장결혈-재관주(I/R)모형조,C조위25 μg/(kg·d)야생형림파독소(rhLTα)치료조,D조위25 μg/ (kg·d)p55TNFR선택성림파독소(rhLTα-Q107E)치료조.각조재제비I/R모형후미량빙지속24h정맥적주생리염수혹치료약물,24h후검측혈장중심기매보(AST、LDH、CK)、양화/항양화지표(SOD、MDA、GSH-Px),초기람사서염색계산심기경사면적.결과 대서심장결혈-재관주(I/R)모형심기경사면적현저증고,심기매보지표、MDA교가수술조명현승고(P<0.05),SOD화GSH-Px칙명현강저(P<0.05).rhLTα-Q107E치료조가역전심기결혈-재관주후심기매보지표、MDA적승고급SOD화GSH-Px적하강(P<0.05),이야생형rhLTα치료조적작용불명현(P>0.05).결론 p5STNFR선택성림파독소대대서심장결혈-재관주후적급성심장손상구유보호작용,기궤제가능통과직접청제양자유기、증가내원성항양화매계통적활력이발휘보호작용.
Objective To investigate the effect of a novel lymphotoxin with selectively binding to p55 tumor necrosis factor receptor (p55TNFR) on myocardial ischemia-reperfusion injury in rats in order to explore the mechanism.Methods A total of 40 SD rats were randomly (random number) assigned into four groups (n =10 in each),namely sham operation group (group A),I/R group (group B),wild type rhLTα treatment group (group C),and p55TNFR selective rhLTα (rhLTα-Q107E) treatment group (group D).After I/R model rats were established,various therapeutic agents or saline were given by continuous intravenous infusion for 24 h via a micropump.After 24 hours of treatment,serum myocardial zymogram,such as aspartate aminotransferase (AST),lactate dehydrogenase (LDH) and creatine kinase (CK),as well as superoxide dismutase (SOD),malondialdehyde (MDA) and glutathione peroxidase (GSH-Px) activities were determined.Myocardial infarction size (MIS) was measured by nitro blue tetrazolium chloride (NBT) staining.Results Compared to sham operation group,MIS,AST,LDH,CK,MDA were increased,while the activities of SOD and GSH-Px were decreased.However,all the effects were significantly reversed by treatment with rhLTα-Q107E (P < 0.05) but not rhLTα (P > 0.05).Conclusions The rhLTα-Q107E plays a role in the protection against myocardial ischemia-reperfusion injury in rats by the mechanism of scavenging oxygen free radicals and increasing the activity of endogenous antioxidant system.