中华麻醉学杂志
中華痳醉學雜誌
중화마취학잡지
CHINESE JOURNAL OF ANESTHESIOLOGY
2011年
7期
871-873
,共3页
曹苏%陈秋萍%康焕菊%沈施仁
曹囌%陳鞦萍%康煥菊%瀋施仁
조소%진추평%강환국%침시인
二氮嗪%心脏%内皮,血管%氧%细胞低氧%1-磷脂酰肌醇3-激酶%蛋白质丝氨酸苏氨酸激酶%RNA,信使
二氮嗪%心髒%內皮,血管%氧%細胞低氧%1-燐脂酰肌醇3-激酶%蛋白質絲氨痠囌氨痠激酶%RNA,信使
이담진%심장%내피,혈관%양%세포저양%1-린지선기순3-격매%단백질사안산소안산격매%RNA,신사
Diazoxide%Heart%Endothelium,vascular%Oxygen%Cell hypoxia%1-Phosphatidylinositol 3-kinase%Protein-serine-threonine kinases%RNA,messenger
目的 评价二氮嗪预先给药对大鼠心肌微血管内皮细胞缺氧复氧时磷脂酰肌醇-3激酶(PI3K) mRNA和蛋白质丝氨酸苏氨酸激酶(Akt) mRNA表达的影响.方法 培养SD大鼠心肌微血管内皮细胞,以1×106个/ml密度接种于96孔培养板(100μl/孔)或培养皿(2 ml/皿),采用随机数字表法,将其随机分为4组(n=25).正常对照组(C组)不作任何处理；缺氧复氧组(H/R组)、二氮嗪预先给药组(DZ组)、二氮嗪预先给药+线粒体ATP敏感性钾通道阻断剂5-羟葵酸组(DZ+ 5-HD组)均进行缺氧2h,复氧2h.DZ组和DZ+ 5-HD组在缺氧前2h分别加入100 μmol/L二氮嗪、100μnol/L二氮嗪+ 100 μmol/L 5-羟葵酸.于复氧2h时测定细胞活力、细胞凋亡率、PI3K mRNA和Akt mRNA表达.结果 与C组比较,H/R组细胞活力降低,细胞凋亡率升高,PI3K mRNA和Akt mRNA表达上调(P＜0.05或0.01)；与H/R组比较,DZ组细胞活力升高,细胞凋亡率降低,PI3K mRNA和Akt mRNA表达上调(P ＜0.05或0.01)；5-羟葵酸可逆转二氮嗪预先给药导致的上述改变(P＜0.05或0.01).结论 二氮嗪预先给药减轻大鼠心肌微血管内皮细胞缺氧复氧损伤的机制与激活线粒体ATP敏感性钾通道,促进PI3K和Akt基因的转录有关.
目的 評價二氮嗪預先給藥對大鼠心肌微血管內皮細胞缺氧複氧時燐脂酰肌醇-3激酶(PI3K) mRNA和蛋白質絲氨痠囌氨痠激酶(Akt) mRNA錶達的影響.方法 培養SD大鼠心肌微血管內皮細胞,以1×106箇/ml密度接種于96孔培養闆(100μl/孔)或培養皿(2 ml/皿),採用隨機數字錶法,將其隨機分為4組(n=25).正常對照組(C組)不作任何處理；缺氧複氧組(H/R組)、二氮嗪預先給藥組(DZ組)、二氮嗪預先給藥+線粒體ATP敏感性鉀通道阻斷劑5-羥葵痠組(DZ+ 5-HD組)均進行缺氧2h,複氧2h.DZ組和DZ+ 5-HD組在缺氧前2h分彆加入100 μmol/L二氮嗪、100μnol/L二氮嗪+ 100 μmol/L 5-羥葵痠.于複氧2h時測定細胞活力、細胞凋亡率、PI3K mRNA和Akt mRNA錶達.結果 與C組比較,H/R組細胞活力降低,細胞凋亡率升高,PI3K mRNA和Akt mRNA錶達上調(P＜0.05或0.01)；與H/R組比較,DZ組細胞活力升高,細胞凋亡率降低,PI3K mRNA和Akt mRNA錶達上調(P ＜0.05或0.01)；5-羥葵痠可逆轉二氮嗪預先給藥導緻的上述改變(P＜0.05或0.01).結論 二氮嗪預先給藥減輕大鼠心肌微血管內皮細胞缺氧複氧損傷的機製與激活線粒體ATP敏感性鉀通道,促進PI3K和Akt基因的轉錄有關.
목적 평개이담진예선급약대대서심기미혈관내피세포결양복양시린지선기순-3격매(PI3K) mRNA화단백질사안산소안산격매(Akt) mRNA표체적영향.방법 배양SD대서심기미혈관내피세포,이1×106개/ml밀도접충우96공배양판(100μl/공)혹배양명(2 ml/명),채용수궤수자표법,장기수궤분위4조(n=25).정상대조조(C조)불작임하처리；결양복양조(H/R조)、이담진예선급약조(DZ조)、이담진예선급약+선립체ATP민감성갑통도조단제5-간규산조(DZ+ 5-HD조)균진행결양2h,복양2h.DZ조화DZ+ 5-HD조재결양전2h분별가입100 μmol/L이담진、100μnol/L이담진+ 100 μmol/L 5-간규산.우복양2h시측정세포활력、세포조망솔、PI3K mRNA화Akt mRNA표체.결과 여C조비교,H/R조세포활력강저,세포조망솔승고,PI3K mRNA화Akt mRNA표체상조(P＜0.05혹0.01)；여H/R조비교,DZ조세포활력승고,세포조망솔강저,PI3K mRNA화Akt mRNA표체상조(P ＜0.05혹0.01)；5-간규산가역전이담진예선급약도치적상술개변(P＜0.05혹0.01).결론 이담진예선급약감경대서심기미혈관내피세포결양복양손상적궤제여격활선립체ATP민감성갑통도,촉진PI3K화Akt기인적전록유관.
Objective To investigate the effects of diazoxide pretreatment on expression of phosphatidylinositol 3-kinase(PI3K) mRNA and protein serine/threonine kinase(Akt) mRNA in rat myocardial microvascular endothelial cells exposed to hypoxia-reoxygenation (H/R).Methods The SD rat myocardial microvascular endothelial cells were cultured.The cells were seeded in 96-well plates ( 100μd/hole) or in 6 cm diameter dishes (2 ml/dish) with the density of 1 × 106/ml and randomly divided into 4 groups ( n =25 each):normal control group (group C),H/R group,diazoxide pretreatment group (group DZ) and diazoxide pretreatment + 5-hydroxydecanoate (5-HD,a mitochondrial ATP-sensitive potassium channel blocker) group (group DZ + 5-HD).The cells were exposed to 2 h hypoxia followed by 2 h reoxygenation.Diazoxide 100 μmol/L and diazoxide 100 μmol/L + 5-HD 100 μmol/L were added to the culture medium 2 h before hypoxia in groups DZ and DZ + 5-HD respectively.The cell viability,apoptotic rate and expression of PI3K mRNA and Akt mRNA were detected at the end of reoxygenation.Results Compared with group C,the cell viability was significantly decreased,while the apoptotic rate increased and expression of PI3K mRNA and Akt mRNA up-regulated in group H/R (P ＜0.05 or 0.01).Compared with group H/R,the cell viability was significantly increased,while the apoptotic rate decreased and expression of PI3K mRNA and Akt mRNA up-regulated in group DZ (P ＜ 0.05 or 0.01).5-HD could inhibit diazoxide pretreatment-induced changes mentioned above (P ＜ 0.05 or 0.01 ).Conclusion Diazoxide pretreatment can reduce H/R injury by promoting PI3K gene and Akt gene transcription through activation of mitochondrial ATP-sensitive potassium channels in rat myocardial microvascular endothelial cells.
