中华急诊医学杂志
中華急診醫學雜誌
중화급진의학잡지
CHINESE JOURNAL OF EMERGENCY MEDICINE
2014年
10期
1105-1108
,共4页
脓毒症%Wistar大鼠%盲肠结扎穿孔术%糖皮质激素%免疫组化%Bcl-2%流式细胞学%心肌细胞凋亡
膿毒癥%Wistar大鼠%盲腸結扎穿孔術%糖皮質激素%免疫組化%Bcl-2%流式細胞學%心肌細胞凋亡
농독증%Wistar대서%맹장결찰천공술%당피질격소%면역조화%Bcl-2%류식세포학%심기세포조망
Sepsis%Wistar rats%Cecal ligation and puncture%Glucocorticoid hormone%Immunhistochemistry%Bcl-2%Flow cytometry%Cardiomyocyte apoptosis
目的 观察脓毒症状态下大鼠心肌细胞凋亡的变化并探讨糖皮质激素对心肌细胞凋亡的影响及其机制,为临床治疗脓毒症心脏损害提供依据.方法 采用盲肠结扎穿孔术制作脓毒症模型.60只体质量为230 ～ 280 g的Wistar大鼠被随机(随机数字法)分为糖皮质激素实验组(n=30)和对照组(n=30).每组大鼠均行盲肠结扎穿孔术,每组术后4h开始给予舒普深200 mg/kg,2次/d.实验组在以上基础上给予地塞米松0.5 mg/kg.每组随机分为3个亚组(6、24、72 h组),于相应时间点取出各组大鼠心脏,分离左心室,制备单细胞悬液,进行流式细胞仪检测心肌细胞凋亡率.使用SPSS 11.5统计软件系统,所有数据以均数±标准差表示((x-)±s),两组间采取独立样本t检验,多组间数据比较采用单因素方差分析.同时左心室行免疫组化检测抗细胞凋亡蛋白B淋巴细胞瘤/白血病-2(B-cell lymphoma/leukemia-2,Bcl-2)的表达.结果 激素组大鼠各时间点心肌细胞凋亡率分别较对照组大鼠心肌细胞凋亡率明显减少(F=9.11,t=5.681,P＜0.01)(6 ht =11.416,P＜0.01;24 h=6.217,P＜0.01;72 h t=3.76,P＜0.01);6h对照组大鼠的心肌细胞凋亡率显著低于24 h及72 h对照组大鼠(F=13.254,sig =0.000,P＜0.01;sig=0.004,P＜0.01);24 h对照组大鼠的心肌细胞凋亡率显著高于72 h对照组大鼠(sig=0.039,P＜0.05);激素各组大鼠心肌细胞凋亡率差异无统计学意义(F=2.488,6/24 h sig=0.132,P＞0.05; 24/72 h sig=0.549,P＞0.05;6/72 h sig=0.053,P＞0.05).结论 脓毒症时存在心肌细胞凋亡,以24 h最明显,脓毒症时应用糖皮质激素能够减少各个阶段心肌细胞凋亡.
目的 觀察膿毒癥狀態下大鼠心肌細胞凋亡的變化併探討糖皮質激素對心肌細胞凋亡的影響及其機製,為臨床治療膿毒癥心髒損害提供依據.方法 採用盲腸結扎穿孔術製作膿毒癥模型.60隻體質量為230 ～ 280 g的Wistar大鼠被隨機(隨機數字法)分為糖皮質激素實驗組(n=30)和對照組(n=30).每組大鼠均行盲腸結扎穿孔術,每組術後4h開始給予舒普深200 mg/kg,2次/d.實驗組在以上基礎上給予地塞米鬆0.5 mg/kg.每組隨機分為3箇亞組(6、24、72 h組),于相應時間點取齣各組大鼠心髒,分離左心室,製備單細胞懸液,進行流式細胞儀檢測心肌細胞凋亡率.使用SPSS 11.5統計軟件繫統,所有數據以均數±標準差錶示((x-)±s),兩組間採取獨立樣本t檢驗,多組間數據比較採用單因素方差分析.同時左心室行免疫組化檢測抗細胞凋亡蛋白B淋巴細胞瘤/白血病-2(B-cell lymphoma/leukemia-2,Bcl-2)的錶達.結果 激素組大鼠各時間點心肌細胞凋亡率分彆較對照組大鼠心肌細胞凋亡率明顯減少(F=9.11,t=5.681,P＜0.01)(6 ht =11.416,P＜0.01;24 h=6.217,P＜0.01;72 h t=3.76,P＜0.01);6h對照組大鼠的心肌細胞凋亡率顯著低于24 h及72 h對照組大鼠(F=13.254,sig =0.000,P＜0.01;sig=0.004,P＜0.01);24 h對照組大鼠的心肌細胞凋亡率顯著高于72 h對照組大鼠(sig=0.039,P＜0.05);激素各組大鼠心肌細胞凋亡率差異無統計學意義(F=2.488,6/24 h sig=0.132,P＞0.05; 24/72 h sig=0.549,P＞0.05;6/72 h sig=0.053,P＞0.05).結論 膿毒癥時存在心肌細胞凋亡,以24 h最明顯,膿毒癥時應用糖皮質激素能夠減少各箇階段心肌細胞凋亡.
목적 관찰농독증상태하대서심기세포조망적변화병탐토당피질격소대심기세포조망적영향급기궤제,위림상치료농독증심장손해제공의거.방법 채용맹장결찰천공술제작농독증모형.60지체질량위230 ～ 280 g적Wistar대서피수궤(수궤수자법)분위당피질격소실험조(n=30)화대조조(n=30).매조대서균행맹장결찰천공술,매조술후4h개시급여서보심200 mg/kg,2차/d.실험조재이상기출상급여지새미송0.5 mg/kg.매조수궤분위3개아조(6、24、72 h조),우상응시간점취출각조대서심장,분리좌심실,제비단세포현액,진행류식세포의검측심기세포조망솔.사용SPSS 11.5통계연건계통,소유수거이균수±표준차표시((x-)±s),량조간채취독립양본t검험,다조간수거비교채용단인소방차분석.동시좌심실행면역조화검측항세포조망단백B림파세포류/백혈병-2(B-cell lymphoma/leukemia-2,Bcl-2)적표체.결과 격소조대서각시간점심기세포조망솔분별교대조조대서심기세포조망솔명현감소(F=9.11,t=5.681,P＜0.01)(6 ht =11.416,P＜0.01;24 h=6.217,P＜0.01;72 h t=3.76,P＜0.01);6h대조조대서적심기세포조망솔현저저우24 h급72 h대조조대서(F=13.254,sig =0.000,P＜0.01;sig=0.004,P＜0.01);24 h대조조대서적심기세포조망솔현저고우72 h대조조대서(sig=0.039,P＜0.05);격소각조대서심기세포조망솔차이무통계학의의(F=2.488,6/24 h sig=0.132,P＞0.05; 24/72 h sig=0.549,P＞0.05;6/72 h sig=0.053,P＞0.05).결론 농독증시존재심기세포조망,이24 h최명현,농독증시응용당피질격소능구감소각개계단심기세포조망.
Objective To observe the occurrence of myocardial apoptosis and discussing the mechanism of the effects of glucocorticoid on myocardial apoptosis in septic rats in order to provide the rationale for clinical strategy.Methods A total of 60 Wistar rats weighing 230-280 g were randomly (random number) divided into control group and experimental group (n =30 in each group).Cecal ligation and puncture (CLP) was performed in rats to induce sepsis,and Cefoperazone Sodium/Sulbactam Sodium (200 mg/kg) was injected into caudal vein 4 hours after CLP,twice a day.In addition,glucocorticoid was given to rats of experimental group.After rats sacrificed,their left ventricular myocardia were rapidly taken out and myocardial apoptosis rate was measured and the level of Bcl-2 was assayed at 6 h,24 h,and 72 h after CLP.Measured data were analyzed with independent-samples t-test and One-Way ANOVA.Results The rates of myocardial apoptosis in experimental group were obviously lower than those in control groups respectively (F=9.11,t=5.681,P＜0.01) (6ht=11.416,P＜0.01; 24ht=6.217,P＜0.01; 72 h t =3.76,P ＜0.01).The rates of myocardial apoptosis in 24 h in control and 72 h control groups were distinctively higher than those in 6 h control group,respectively (F =13.254,sig =0.000,P ＜0.01 ; sig =0.004,P ＜ 0.01).The rates ofmyocardial apoptosis in group 24 h control were higher than those in 72 h control group (sig =0.039,P ＜ 0.05).The rates of myocardial apoptosis make no difference among experimental group (F =2.488,6/24 h sig =0.132,P ＞ 0.05 ; 24/72 h sig =0.549,P ＞ 0.05 ; 6/72 h sig =0.053,P ＞ 0.05).Conclusions The rate of myocardial apoptosis is peaked at 24 h in sepsis rat,and the rate of myocardial apoptosis can be obviously decreased by administration of glucocorticoid.
