中华麻醉学杂志
中華痳醉學雜誌
중화마취학잡지
CHINESE JOURNAL OF ANESTHESIOLOGY
2010年
11期
1394-1396
,共3页
曹苏%康焕菊%陈秋萍%沈施仁
曹囌%康煥菊%陳鞦萍%瀋施仁
조소%강환국%진추평%침시인
二氮嗪%心脏%内皮,血管%氧%细胞低氧%NF-Κb%趋化因子CX3CL1
二氮嗪%心髒%內皮,血管%氧%細胞低氧%NF-Κb%趨化因子CX3CL1
이담진%심장%내피,혈관%양%세포저양%NF-Κb%추화인자CX3CL1
Dazoxide%Heart%Endothelium,vascular%Oxygen%Cell hpoxia%NF-kappa B%Chemokine CX3CL1
目的 探讨二氮嗪预先给药对大鼠心肌微血管内皮细胞缺氧复氧时NF-κB mRNA和fractalkine(FKN)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的密度接种于96孔板(100μl/孔)或培养皿(2 ml/皿),随机分为4组(n=24).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2 h、复氧2 h.DZ组和DZ+5-HD组在缺氧前2 h分别加入100 μmol/L二氮嗪、100 μmol/L二氮嗪+100μmol/L 5-羟葵酸.于复氧2 h时测定细胞活力、细胞凋亡率、NF-κB mRNA和FKN mRNA表达水平.结果 与C组比较,H/R组细胞活力降低,细胞凋亡率升高,NF-κB mRNA和FKN mRNA表达上调(P＜0.01);与H/R组比较,DZ组细胞活力升高,细胞凋亡率降低,NF-κB mRNA和FKN mRNA表达下调(P＜0.05);5-羟葵酸可抑制二氮嗪预先给药导致的上述改变(P＜0.05).结论 二氮嗪预先给药可下调NF-κB和FKN表达,从而减轻大鼠心肌微血管内皮细胞缺氧复氧损伤,其机制与激活线粒体ATP敏感性钾通道有关.
目的 探討二氮嗪預先給藥對大鼠心肌微血管內皮細胞缺氧複氧時NF-κB mRNA和fractalkine(FKN)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的密度接種于96孔闆(100μl/孔)或培養皿(2 ml/皿),隨機分為4組(n=24).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2 h、複氧2 h.DZ組和DZ+5-HD組在缺氧前2 h分彆加入100 μmol/L二氮嗪、100 μmol/L二氮嗪+100μmol/L 5-羥葵痠.于複氧2 h時測定細胞活力、細胞凋亡率、NF-κB mRNA和FKN mRNA錶達水平.結果 與C組比較,H/R組細胞活力降低,細胞凋亡率升高,NF-κB mRNA和FKN mRNA錶達上調(P＜0.01);與H/R組比較,DZ組細胞活力升高,細胞凋亡率降低,NF-κB mRNA和FKN mRNA錶達下調(P＜0.05);5-羥葵痠可抑製二氮嗪預先給藥導緻的上述改變(P＜0.05).結論 二氮嗪預先給藥可下調NF-κB和FKN錶達,從而減輕大鼠心肌微血管內皮細胞缺氧複氧損傷,其機製與激活線粒體ATP敏感性鉀通道有關.
목적 탐토이담진예선급약대대서심기미혈관내피세포결양복양시NF-κB mRNA화fractalkine(FKN)mRNA표체적영향.방법 배양SD대서심기미혈관내피세포,이1×106개/ml적밀도접충우96공판(100μl/공)혹배양명(2 ml/명),수궤분위4조(n=24).정상대조조(C조)불작임하처리,결양복양조(H/R조)、이담진예선급약조(DZ조)、이담진예선급약+선립체ATP민감성갑통도조단제5-간규산조(DZ+5-HD조)균진행결양2 h、복양2 h.DZ조화DZ+5-HD조재결양전2 h분별가입100 μmol/L이담진、100 μmol/L이담진+100μmol/L 5-간규산.우복양2 h시측정세포활력、세포조망솔、NF-κB mRNA화FKN mRNA표체수평.결과 여C조비교,H/R조세포활력강저,세포조망솔승고,NF-κB mRNA화FKN mRNA표체상조(P＜0.01);여H/R조비교,DZ조세포활력승고,세포조망솔강저,NF-κB mRNA화FKN mRNA표체하조(P＜0.05);5-간규산가억제이담진예선급약도치적상술개변(P＜0.05).결론 이담진예선급약가하조NF-κB화FKN표체,종이감경대서심기미혈관내피세포결양복양손상,기궤제여격활선립체ATP민감성갑통도유관.
Objective To investigate the effects of diazoxide pretreatment on the expression of NF-κB mRNA and fractalkine (FKN) 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 (100μl/hole) or in 6 cm diameter dishes (2 ml/dish) with the density of 1 × 106/ml and randomly divided into4 groups (n = 24 each): Ⅰ normal control group (group C), Ⅱ H/R group, Ⅲ diazoxide pretreatment group (group DZ), Ⅳ diazoxide pretreatment + mitochondrial ATP-sensitive potassium channel blocker 5-hydroxydecanoate (5-HD) 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 100μmol/L were added to the cultured medium 2 h before hypoxia in group DZ and DZ + 5-HD respectively. The cell vitality, apoptotic rate and expression of NF-κB mRNA and FKN mRNA were detected at end of reoxygenation. Results Compared with group C, the cell vitality was significantly decreased, apoptotic rate increased and the expression of NF-κB mRNA and FKN mRNA up-regulated in H/R group. Compared with group H/R, the cell vitality was significantly increased,apoptotic rate decreased and the expression of NF-κB mRNA and FKN mRNA down-regulated in group DZ. 5-HD could inhibit diazoxide pretreatment-induced changes mentioned above. Conclusion Diazoxide pretreatment can reduce H/R injury in rat myocardial microvascular endothelial cells through down-regulating the expression of NFκB and FKN, and the mechanism is related to activation of mitochondrial ATP-sensitive potassium channels.
