中华麻醉学杂志
中華痳醉學雜誌
중화마취학잡지
CHINESE JOURNAL OF ANESTHESIOLOGY
2010年
3期
365-368
,共4页
二异丙酚%肺栓塞%细胞凋亡%肺
二異丙酚%肺栓塞%細胞凋亡%肺
이이병분%폐전새%세포조망%폐
Propofol%Pulmonary embolism%Apoptosis%Lung
目的 评价异丙酚对急性肺栓塞大鼠肺细胞凋亡的影响.方法 健康雄性SD大鼠40只,体重280～300 g,随机分为5组(n=8):假手术组(S组)、急性肺栓塞组(APTE组)、异丙酚4 mg·kg-1 ·h-1 组(P1组)、异丙酚8 mg·kg-1 ·h- 1组(P2组)和异丙酚16 mg·kg-1 ·h-1 组(P3组).取尾静脉血样0.2 ml,37℃水浴箱内过夜,分割成直径1 mm ,长5 mm的栓子,颈静脉注射混有15个栓子的2 ml生理盐水制备大鼠肺栓塞模型.S组静脉输注生理盐水2 ml/h 4 h;APTE组、P1组、P2组和P3组制备肺栓塞模型,然后APTE组静脉输注5%葡萄糖2 ml/h4 h,P1 组、P2组和P3组分别静脉输注异丙酚4、8、16 mg·kg-1 ·h-1 (用5%葡萄糖稀释至2 m1)4 h.给药结束后,处死大鼠,取肺组织,采用流式细胞仪检测细胞凋亡情况,计算细胞凋亡率,采用RT-PCR法检测caspase-3、Bcl-2、Box、Fas和FasL的mRNA表达水平,采用Western blot法检测caspase-3、Bcl-2、Bax、Fas和FasL的蛋白表达水平,计算Bcl-2/Bax的mRNA和蛋白表达比值.结果 与S组比较,AVIE组、P1组、P2组和P3 组肺组织细胞凋亡率升高,caspase-3、Bax、Fas、FasL的mRNA和蛋白表达上调,Bcl-2的mRNA和蛋白表达下调,Bcl-2/Bax的mRNA和蛋白表达比值降低(P＜0.05或0.01);与APTE组比较,P1组、P2组和P3 组肺组织细胞凋亡率降低,caspase-3、Bax、Fas、FasL的mRNA和蛋白表达下调,Bcl-2的mRNA和蛋白表达上调,Bcl-2/Bax的mRNA和蛋白表达比值升高(P＜0.05或0.01);P.组、P2组和P3组间肺组织细胞凋亡率、caspase-3、Bcl-2、Bax、Fas、 FasL的mRNA和蛋白表达、Bcl-2/Bax的mRNA和蛋白表达比值差异无统计学意义(P＞0.05).结论 异丙酚可抑制急性肺栓塞大鼠肺细胞凋亡,其机制与下调肺组织caspase-3、Fas和FasL的表达,调节Bcl-2/Bax的平衡有关.
目的 評價異丙酚對急性肺栓塞大鼠肺細胞凋亡的影響.方法 健康雄性SD大鼠40隻,體重280～300 g,隨機分為5組(n=8):假手術組(S組)、急性肺栓塞組(APTE組)、異丙酚4 mg·kg-1 ·h-1 組(P1組)、異丙酚8 mg·kg-1 ·h- 1組(P2組)和異丙酚16 mg·kg-1 ·h-1 組(P3組).取尾靜脈血樣0.2 ml,37℃水浴箱內過夜,分割成直徑1 mm ,長5 mm的栓子,頸靜脈註射混有15箇栓子的2 ml生理鹽水製備大鼠肺栓塞模型.S組靜脈輸註生理鹽水2 ml/h 4 h;APTE組、P1組、P2組和P3組製備肺栓塞模型,然後APTE組靜脈輸註5%葡萄糖2 ml/h4 h,P1 組、P2組和P3組分彆靜脈輸註異丙酚4、8、16 mg·kg-1 ·h-1 (用5%葡萄糖稀釋至2 m1)4 h.給藥結束後,處死大鼠,取肺組織,採用流式細胞儀檢測細胞凋亡情況,計算細胞凋亡率,採用RT-PCR法檢測caspase-3、Bcl-2、Box、Fas和FasL的mRNA錶達水平,採用Western blot法檢測caspase-3、Bcl-2、Bax、Fas和FasL的蛋白錶達水平,計算Bcl-2/Bax的mRNA和蛋白錶達比值.結果 與S組比較,AVIE組、P1組、P2組和P3 組肺組織細胞凋亡率升高,caspase-3、Bax、Fas、FasL的mRNA和蛋白錶達上調,Bcl-2的mRNA和蛋白錶達下調,Bcl-2/Bax的mRNA和蛋白錶達比值降低(P＜0.05或0.01);與APTE組比較,P1組、P2組和P3 組肺組織細胞凋亡率降低,caspase-3、Bax、Fas、FasL的mRNA和蛋白錶達下調,Bcl-2的mRNA和蛋白錶達上調,Bcl-2/Bax的mRNA和蛋白錶達比值升高(P＜0.05或0.01);P.組、P2組和P3組間肺組織細胞凋亡率、caspase-3、Bcl-2、Bax、Fas、 FasL的mRNA和蛋白錶達、Bcl-2/Bax的mRNA和蛋白錶達比值差異無統計學意義(P＞0.05).結論 異丙酚可抑製急性肺栓塞大鼠肺細胞凋亡,其機製與下調肺組織caspase-3、Fas和FasL的錶達,調節Bcl-2/Bax的平衡有關.
목적 평개이병분대급성폐전새대서폐세포조망적영향.방법 건강웅성SD대서40지,체중280～300 g,수궤분위5조(n=8):가수술조(S조)、급성폐전새조(APTE조)、이병분4 mg·kg-1 ·h-1 조(P1조)、이병분8 mg·kg-1 ·h- 1조(P2조)화이병분16 mg·kg-1 ·h-1 조(P3조).취미정맥혈양0.2 ml,37℃수욕상내과야,분할성직경1 mm ,장5 mm적전자,경정맥주사혼유15개전자적2 ml생리염수제비대서폐전새모형.S조정맥수주생리염수2 ml/h 4 h;APTE조、P1조、P2조화P3조제비폐전새모형,연후APTE조정맥수주5%포도당2 ml/h4 h,P1 조、P2조화P3조분별정맥수주이병분4、8、16 mg·kg-1 ·h-1 (용5%포도당희석지2 m1)4 h.급약결속후,처사대서,취폐조직,채용류식세포의검측세포조망정황,계산세포조망솔,채용RT-PCR법검측caspase-3、Bcl-2、Box、Fas화FasL적mRNA표체수평,채용Western blot법검측caspase-3、Bcl-2、Bax、Fas화FasL적단백표체수평,계산Bcl-2/Bax적mRNA화단백표체비치.결과 여S조비교,AVIE조、P1조、P2조화P3 조폐조직세포조망솔승고,caspase-3、Bax、Fas、FasL적mRNA화단백표체상조,Bcl-2적mRNA화단백표체하조,Bcl-2/Bax적mRNA화단백표체비치강저(P＜0.05혹0.01);여APTE조비교,P1조、P2조화P3 조폐조직세포조망솔강저,caspase-3、Bax、Fas、FasL적mRNA화단백표체하조,Bcl-2적mRNA화단백표체상조,Bcl-2/Bax적mRNA화단백표체비치승고(P＜0.05혹0.01);P.조、P2조화P3조간폐조직세포조망솔、caspase-3、Bcl-2、Bax、Fas、 FasL적mRNA화단백표체、Bcl-2/Bax적mRNA화단백표체비치차이무통계학의의(P＞0.05).결론 이병분가억제급성폐전새대서폐세포조망,기궤제여하조폐조직caspase-3、Fas화FasL적표체,조절Bcl-2/Bax적평형유관.
Objective To evaluate the effect of propofol on lung cell apoptosis induced by acute pulmonary thromboembolism (APTE) .Methods Forty male SD rats weighing 280-300 g were randomly divided into 5 groups ( n = 8 each) : group Ⅰ sham operation ( group S) ; group ⅡAPTE and 3 propofol groups ( group P1-3). APTE was produced by iv injection of auto-blood clots. Venous blood 0.2 ml was obtained from rat tail vein and placed in a sterile test tube which was kept in water bath at 37 ℃ overnight. The blood clot was cut into thrombi ( diameter 1 mm, length 5 mm) the next day. Fifteen thrombi in 2 ml of normal saline were injected into immediately after iv injection of auto-bloed clots. The animals were killed at the end of 4 h propofol infusion and lung specimens were obtained for determination of lung cell apoptosis rate by flow eytometry and expression of caspase-3, Bax, Bcl-2, Fas, FasL mRNA and protein by RT-PCR and Western blot.The expression of Bcl-2/Bax mRNA and protein was calculated. Results Compared with group S,APTE significantly increased the lung cell apoptosis rate, and expression of caspase-3, Bax, Fas, FasL and decreased the expression of Bcl-2 and Bcl-2/Bax. Propofol infusion significantly attenuated these APTE-induced changes. Conclusion Propofol can inhibit APTE-induced lung cell apoptosis by down-regulating the caspase-3, Fas and FasL expression and regulating the balance between Bcl-2 and Bax expression.
