中国危重病急救医学
中國危重病急救醫學
중국위중병급구의학
CHINESE CRITICAL CARE MEDICINE
2011年
12期
714-717
,共4页
吕根法%石宏伟%樊磊%冯忠明%王光远
呂根法%石宏偉%樊磊%馮忠明%王光遠
려근법%석굉위%번뢰%풍충명%왕광원
烫伤%胰岛素强化治疗%心肌细胞%凋亡
燙傷%胰島素彊化治療%心肌細胞%凋亡
탕상%이도소강화치료%심기세포%조망
Burn%Intensive insulin treatment%Myocardium%Apoptosis
目的 探讨大鼠重度烫伤后胰岛素强化治疗拮抗心肌细胞凋亡的作用及机制.方法 将18只SD大鼠按随机数字表法分为假伤组、烫伤组和胰岛素强化治疗组(强化治疗组),每组6只.制作30％总体表面积(TBSA)Ⅱ度烫伤模型及胰岛素强化治疗模型.伤后6h取大鼠左室心肌组织,采用原位末端缺刻标记法(TUNEL)检测心肌细胞凋亡,用免疫组化和蛋白质免疫印迹法(Western blotting)分别观察3种凋亡相关基因天冬氨酸特异性半胱氨酸蛋白酶3(caspase-3)、Bax和Bcl-2的蛋白表达.结果 与假伤组比较,烫伤后心肌凋亡细胞明显增多[(13.1±3.4)％比(0.6±0.4)％,P＜0.01];caspase-3、Bax的蛋白表达明显增高(免疫组化caspase-3:13.72±4.13比1.36±0.95,Bax:29.64±5.42比2.24±1.04; Western blotting caspase-3:5.72±2.13比1,Bax:4.64±1.42比1),而Bcl-2表达水平显著降低(免疫组化:3.39±1.52比8.01±2.56；Western blotting:0.69±0.42比1,均P＜0.01).经胰岛素强化治疗后,心肌细胞的凋亡率较烫伤组明显降低[(6.7±1.8)％比(13.1±3.4)％,P＜0.01],3种凋亡相关基因的蛋白表达水平正好与烫伤组的变化相反(免疫组化caspase-3:8.88±3.36比13.72±4.13,Bax:14.43±3.69比29.64±5.42,Bcl-2:8.61±3.72比3.39±1.52；Western blotting caspase-3:2.18±0.86比5.72±2.13,Bax:2.87±1.35比4.64±1.42,Bcl-2:3.57±1.70比0.69±0.42,P＜0.05或P＜0.01).结论胰岛素强化治疗可能通过调节caspase-3、Bax和Bcl-2 3种细胞凋亡相关基因的表达,对烫伤后心肌细胞发挥抗凋亡作用.
目的 探討大鼠重度燙傷後胰島素彊化治療拮抗心肌細胞凋亡的作用及機製.方法 將18隻SD大鼠按隨機數字錶法分為假傷組、燙傷組和胰島素彊化治療組(彊化治療組),每組6隻.製作30％總體錶麵積(TBSA)Ⅱ度燙傷模型及胰島素彊化治療模型.傷後6h取大鼠左室心肌組織,採用原位末耑缺刻標記法(TUNEL)檢測心肌細胞凋亡,用免疫組化和蛋白質免疫印跡法(Western blotting)分彆觀察3種凋亡相關基因天鼕氨痠特異性半胱氨痠蛋白酶3(caspase-3)、Bax和Bcl-2的蛋白錶達.結果 與假傷組比較,燙傷後心肌凋亡細胞明顯增多[(13.1±3.4)％比(0.6±0.4)％,P＜0.01];caspase-3、Bax的蛋白錶達明顯增高(免疫組化caspase-3:13.72±4.13比1.36±0.95,Bax:29.64±5.42比2.24±1.04; Western blotting caspase-3:5.72±2.13比1,Bax:4.64±1.42比1),而Bcl-2錶達水平顯著降低(免疫組化:3.39±1.52比8.01±2.56；Western blotting:0.69±0.42比1,均P＜0.01).經胰島素彊化治療後,心肌細胞的凋亡率較燙傷組明顯降低[(6.7±1.8)％比(13.1±3.4)％,P＜0.01],3種凋亡相關基因的蛋白錶達水平正好與燙傷組的變化相反(免疫組化caspase-3:8.88±3.36比13.72±4.13,Bax:14.43±3.69比29.64±5.42,Bcl-2:8.61±3.72比3.39±1.52；Western blotting caspase-3:2.18±0.86比5.72±2.13,Bax:2.87±1.35比4.64±1.42,Bcl-2:3.57±1.70比0.69±0.42,P＜0.05或P＜0.01).結論胰島素彊化治療可能通過調節caspase-3、Bax和Bcl-2 3種細胞凋亡相關基因的錶達,對燙傷後心肌細胞髮揮抗凋亡作用.
목적 탐토대서중도탕상후이도소강화치료길항심기세포조망적작용급궤제.방법 장18지SD대서안수궤수자표법분위가상조、탕상조화이도소강화치료조(강화치료조),매조6지.제작30％총체표면적(TBSA)Ⅱ도탕상모형급이도소강화치료모형.상후6h취대서좌실심기조직,채용원위말단결각표기법(TUNEL)검측심기세포조망,용면역조화화단백질면역인적법(Western blotting)분별관찰3충조망상관기인천동안산특이성반광안산단백매3(caspase-3)、Bax화Bcl-2적단백표체.결과 여가상조비교,탕상후심기조망세포명현증다[(13.1±3.4)％비(0.6±0.4)％,P＜0.01];caspase-3、Bax적단백표체명현증고(면역조화caspase-3:13.72±4.13비1.36±0.95,Bax:29.64±5.42비2.24±1.04; Western blotting caspase-3:5.72±2.13비1,Bax:4.64±1.42비1),이Bcl-2표체수평현저강저(면역조화:3.39±1.52비8.01±2.56；Western blotting:0.69±0.42비1,균P＜0.01).경이도소강화치료후,심기세포적조망솔교탕상조명현강저[(6.7±1.8)％비(13.1±3.4)％,P＜0.01],3충조망상관기인적단백표체수평정호여탕상조적변화상반(면역조화caspase-3:8.88±3.36비13.72±4.13,Bax:14.43±3.69비29.64±5.42,Bcl-2:8.61±3.72비3.39±1.52；Western blotting caspase-3:2.18±0.86비5.72±2.13,Bax:2.87±1.35비4.64±1.42,Bcl-2:3.57±1.70비0.69±0.42,P＜0.05혹P＜0.01).결론이도소강화치료가능통과조절caspase-3、Bax화Bcl-2 3충세포조망상관기인적표체,대탕상후심기세포발휘항조망작용.
Objective To investigate the effect of intensive insulin treatment,in the protection of myocardiocytes against apoptosis in severely scalded rats and its underlying mechanism.Methods Eighteen Sprague-Dawley(SD)rats were randomly divided into three groups(6/each)to receive:sham surgery,burn damage(on the back of the animals,degree Ⅱ,to 30％ of total body surface area),and burn damage± intensive insulin treatment.Tissue samples were collected from the left ventricle 6 hours after infliction of the burn damage for the examination of myocardial cell apoptosis[by terminal-deoxynucleoitidyl transferase mediated nick end labeling(TUNEL)staining]and the expression of apoptosis-related molecules caspase-3,Bax,and Bcl-2(by immuno-histochemistry and Western blotting).Results In comparison with the animals in sham treated group,the myocardiocyte apoptosis rate in animals in burn damage only group increased significantly[(13.1 ± 3.4)％ vs.(0.6 ± 0.4)％,P ＜ 0.01].The expression of caspase-3 and Bax both significantly increased while the level of Bcl-2 expression significantly decreased(immuno-histochemistry caspase-3:13.72±4.13 vs.1.36±0.95,Bax:29.64±5.42 vs.2.24±1.04,Bcl-2:3.39±1.52 vs.8.01± 2.56; Western blotting caspase-3:5.72±±2.13 vs.1,Bax:4.64±1.42 vs.1,Bcl2:0.69±0.42 vs.1,all P＜0.01).The animals received intensive insulin treatment showed significantly less myocardiocyte apoptosis [(6.7 ± 1.8)％ vs.(13.1 ± 3.4)％,P ＜ 0.01],significantly lower expression in caspase-3,Bax,and significantly higher level of Bcl-2 expression as compared to the animals in burn damage only group (immuno-histochemistry caspase-3:8.88 ± 3.36 vs.13.72 ± 4.13,Bax:14.43 ± 3.69 vs.29.64 ± 5.42,Bcl-2:8.61±3.72 vs.3.39±1.52; Western blotting caspase-3:2.18±0.86 vs.5.72±2.13,Bax:2.87± 1.35vs.4.64±1.42,Bcl-2:3.57±1.70vs.0.69±0.42,P＜0.05 or P＜0.01).Conclusion Intensive insulin therapy may protect myocardiocytes against apoptosis in severely burned animals through the regulation of the expression of apoptosis-related molecules caspase-3,Bax and Bcl-2.
