国际免疫学杂志
國際免疫學雜誌
국제면역학잡지
INTERNATIONAL JOURNAL OF IMMUNOLOGY
2015年
3期
229-233
,共5页
郭艳祥%隋海静%李冬梅%丁文刚%林长赋
郭豔祥%隋海靜%李鼕梅%丁文剛%林長賦
곽염상%수해정%리동매%정문강%림장부
丙泊酚%心肌%缺血再灌注损伤%2型糖尿病%内皮细胞
丙泊酚%心肌%缺血再灌註損傷%2型糖尿病%內皮細胞
병박분%심기%결혈재관주손상%2형당뇨병%내피세포
Propofol%Myocardium%Ischemia reperfusion injury%Type 2 diabetes mellitus%Endothelial cells
目的 探讨丙泊酚(propofol)对2型糖尿病大鼠心肌缺血再灌注损伤期间内皮细胞功能的影响.方法 雄性Wistar大鼠48只,随机分为糖尿病组(D组)和非糖尿病对照组(N组),两组各24只.N组随机分为三组(每组8只),即心肌缺血再灌注组(NI组)、心肌缺血再灌注+丙泊酚组(NP组)、假手术组(NS组);D组随机分为三组(每组8只),即糖尿病心肌缺血再灌注组(DI组)、糖尿病心肌缺血再灌注+丙泊酚组(DP组)、糖尿病假手术组(DS组).采用高脂高糖饮食联合腹腔注射链脲佐菌素(STZ)方法制备2型糖尿病模型.DI组和NI组采用结扎左冠状动脉前降支30 min再灌注2h的方法制备心肌缺血再灌注模型.DP组、NP组在缺血前10 min开始静脉泵注丙泊白酚6 mg· kg-1·h-1至再灌注2h结束,DI组、NI组给予等容量的生理盐水;DS组、NS组仅穿线不结扎.再灌注结束后,取部分病变心肌,光镜下观察缺血心肌形态学改变,测定基础状态、再灌注结束后血清中一氧化氮(NO)、内皮素-1(ET-1)的含量.结果 NI组与NS组比较,NI组NO水平降低、ET-1水平升高(F=12.18、14.37,P ＜0.05).与NI组比较,NP组NO水平升高、ET-1水平降低(F=14.99、15.521,P＜0.05).DI组与DS组比较,DI组NO水平降低、ET-1水平升高(F=4.76、4.94,P＜0.05),与DI组比较,DP组NO水平明显升高、ET-1水平降低显著(F=6.40、8.80,P＜0.05).结论 丙泊酚能改善心肌内皮细胞功能,减轻2型糖尿病大鼠心肌缺血再灌注损伤.
目的 探討丙泊酚(propofol)對2型糖尿病大鼠心肌缺血再灌註損傷期間內皮細胞功能的影響.方法 雄性Wistar大鼠48隻,隨機分為糖尿病組(D組)和非糖尿病對照組(N組),兩組各24隻.N組隨機分為三組(每組8隻),即心肌缺血再灌註組(NI組)、心肌缺血再灌註+丙泊酚組(NP組)、假手術組(NS組);D組隨機分為三組(每組8隻),即糖尿病心肌缺血再灌註組(DI組)、糖尿病心肌缺血再灌註+丙泊酚組(DP組)、糖尿病假手術組(DS組).採用高脂高糖飲食聯閤腹腔註射鏈脲佐菌素(STZ)方法製備2型糖尿病模型.DI組和NI組採用結扎左冠狀動脈前降支30 min再灌註2h的方法製備心肌缺血再灌註模型.DP組、NP組在缺血前10 min開始靜脈泵註丙泊白酚6 mg· kg-1·h-1至再灌註2h結束,DI組、NI組給予等容量的生理鹽水;DS組、NS組僅穿線不結扎.再灌註結束後,取部分病變心肌,光鏡下觀察缺血心肌形態學改變,測定基礎狀態、再灌註結束後血清中一氧化氮(NO)、內皮素-1(ET-1)的含量.結果 NI組與NS組比較,NI組NO水平降低、ET-1水平升高(F=12.18、14.37,P ＜0.05).與NI組比較,NP組NO水平升高、ET-1水平降低(F=14.99、15.521,P＜0.05).DI組與DS組比較,DI組NO水平降低、ET-1水平升高(F=4.76、4.94,P＜0.05),與DI組比較,DP組NO水平明顯升高、ET-1水平降低顯著(F=6.40、8.80,P＜0.05).結論 丙泊酚能改善心肌內皮細胞功能,減輕2型糖尿病大鼠心肌缺血再灌註損傷.
목적 탐토병박분(propofol)대2형당뇨병대서심기결혈재관주손상기간내피세포공능적영향.방법 웅성Wistar대서48지,수궤분위당뇨병조(D조)화비당뇨병대조조(N조),량조각24지.N조수궤분위삼조(매조8지),즉심기결혈재관주조(NI조)、심기결혈재관주+병박분조(NP조)、가수술조(NS조);D조수궤분위삼조(매조8지),즉당뇨병심기결혈재관주조(DI조)、당뇨병심기결혈재관주+병박분조(DP조)、당뇨병가수술조(DS조).채용고지고당음식연합복강주사련뇨좌균소(STZ)방법제비2형당뇨병모형.DI조화NI조채용결찰좌관상동맥전강지30 min재관주2h적방법제비심기결혈재관주모형.DP조、NP조재결혈전10 min개시정맥빙주병박백분6 mg· kg-1·h-1지재관주2h결속,DI조、NI조급여등용량적생리염수;DS조、NS조부천선불결찰.재관주결속후,취부분병변심기,광경하관찰결혈심기형태학개변,측정기출상태、재관주결속후혈청중일양화담(NO)、내피소-1(ET-1)적함량.결과 NI조여NS조비교,NI조NO수평강저、ET-1수평승고(F=12.18、14.37,P ＜0.05).여NI조비교,NP조NO수평승고、ET-1수평강저(F=14.99、15.521,P＜0.05).DI조여DS조비교,DI조NO수평강저、ET-1수평승고(F=4.76、4.94,P＜0.05),여DI조비교,DP조NO수평명현승고、ET-1수평강저현저(F=6.40、8.80,P＜0.05).결론 병박분능개선심기내피세포공능,감경2형당뇨병대서심기결혈재관주손상.
Objective To evaluate the effects of propofol on the function of endothelial cells during myocardial ischemia reperfusion(I/R) injury in type 2 diabetic rats.Methods 48 male Wistar rats were randomly divided into two groups,nondiabetic control group(N group,n =24) and diabetic group (D group,n =24).The N group was randomly divided into three groups (n =8):I/R group(NI),I/R + propofol group (NP),sham group(NS).D group was randomly divided into three groups(n =8):diabetic I/R group(DI),diabetic I/R + propofol group(DP),diabetic sham group(DS).We developed a rat model by supplying the male Wistar rats with high-fat diet following low-dose STZ as type 2 diabetic rats.The cardial I/R was established by ligaturing left anterior descending coronary artery(LAD) for 30 minutes and reperfusing for 2 hours in DI and NI groups.Group DS and NS were just threaded without being ligatured.Group DP and NP were pumped with propofol 6 mg · kg-1 · h-1 from 10 min before ischemia to the end of reperfusion.The pathological changes of myocardium were examined by light microscopy.Under basal state and the moment after 2 h's reperfusion,NO and ET-1 in the serum were measured.Results Compared with NS group,the content of NO decreased while ET-1 increased in the plasma 2 h after reperfusion in NI group (P ＜ 0.05).Compared with NI group,NO increased while ET-1 decreased in NP group.Compared with DS group,NO decreased while ET-1 increased in the plasma at 2 h after reperfusion in DI group (P ＜ 0.05).Compared with DI group,NO increased while ET-1 decreased in the plasma 2 h after reperfusion in DP group (P ＜ 0.05).Conclusion Propofol showed myocardial 2 h protective effect against the ischemia reperfusion injury via improving the function of endothelial cells in type 2 diabetic rats.
