中国药物应用与监测
中國藥物應用與鑑測
중국약물응용여감측
CHINESE JOURNAL OF DRUG APPLICATION AND MONITORING
2013年
5期
258-260
,共3页
莫晓飞%陈刘芳%万晶%吴云%柯剑娟
莫曉飛%陳劉芳%萬晶%吳雲%柯劍娟
막효비%진류방%만정%오운%가검연
缺血再灌注%补体3%右美托咪定
缺血再灌註%補體3%右美託咪定
결혈재관주%보체3%우미탁미정
Ischemic-reperfusion%Complement component 3%Dexmedetomidine
目的：：探讨右美托咪定预处理对大鼠心肌缺血再灌注损伤的保护作用及对补体3（C3）蛋白的影响。方法：SD雄性大鼠45只，随机分为3组（n=15）：假手术组（Sham组）、缺血再灌注组（I/R组）、右美托咪定预处理组（DEX组）。DEX组自缺血前2 h持续静脉输注右美托咪定5 mL· kg-1（用0.9％氯化钠注射液将右美托咪定稀释为1μg· mL-1）直到结扎心脏冠状动脉左前降支前停止，输注时间为2 h；Sham组及I/R组在相同的时间内按照5 mL· kg-1速率输注等量0.9％氯化钠注射液。再灌注120 min时，取心脏组织，测定心肌梗死面积，用蛋白质印迹法（Western blot）测定心肌组织中C3蛋白的表达。结果：与Sham组比较，I/R组和DEX组的心肌梗死面积、C3蛋白表达明显升高（P <0.05)；与I/R组比较，DEX组的心肌梗死面积和C3蛋白表达明显降低（P<0.05)。结论：右美托咪定预处理能够减轻大鼠心肌缺血再灌注损伤，其机制与减少补体3蛋白表达有关。
目的：：探討右美託咪定預處理對大鼠心肌缺血再灌註損傷的保護作用及對補體3（C3）蛋白的影響。方法：SD雄性大鼠45隻，隨機分為3組（n=15）：假手術組（Sham組）、缺血再灌註組（I/R組）、右美託咪定預處理組（DEX組）。DEX組自缺血前2 h持續靜脈輸註右美託咪定5 mL· kg-1（用0.9％氯化鈉註射液將右美託咪定稀釋為1μg· mL-1）直到結扎心髒冠狀動脈左前降支前停止，輸註時間為2 h；Sham組及I/R組在相同的時間內按照5 mL· kg-1速率輸註等量0.9％氯化鈉註射液。再灌註120 min時，取心髒組織，測定心肌梗死麵積，用蛋白質印跡法（Western blot）測定心肌組織中C3蛋白的錶達。結果：與Sham組比較，I/R組和DEX組的心肌梗死麵積、C3蛋白錶達明顯升高（P <0.05)；與I/R組比較，DEX組的心肌梗死麵積和C3蛋白錶達明顯降低（P<0.05)。結論：右美託咪定預處理能夠減輕大鼠心肌缺血再灌註損傷，其機製與減少補體3蛋白錶達有關。
목적：：탐토우미탁미정예처리대대서심기결혈재관주손상적보호작용급대보체3（C3）단백적영향。방법：SD웅성대서45지，수궤분위3조（n=15）：가수술조（Sham조）、결혈재관주조（I/R조）、우미탁미정예처리조（DEX조）。DEX조자결혈전2 h지속정맥수주우미탁미정5 mL· kg-1（용0.9％록화납주사액장우미탁미정희석위1μg· mL-1）직도결찰심장관상동맥좌전강지전정지，수주시간위2 h；Sham조급I/R조재상동적시간내안조5 mL· kg-1속솔수주등량0.9％록화납주사액。재관주120 min시，취심장조직，측정심기경사면적，용단백질인적법（Western blot）측정심기조직중C3단백적표체。결과：여Sham조비교，I/R조화DEX조적심기경사면적、C3단백표체명현승고（P <0.05)；여I/R조비교，DEX조적심기경사면적화C3단백표체명현강저（P<0.05)。결론：우미탁미정예처리능구감경대서심기결혈재관주손상，기궤제여감소보체3단백표체유관。
Objective:To investigate the protective effect and possible mechanism (effect on complement component 3) of dexmedetomidine preconditioning on the myocardium of ischemia and reperfused rats. Methods:Forty-five Sprague-Dawley male rats were divided into sham operation group(Sham group), ischemic-reperfusion group (I/R group) and dexmedetomidine preconditioning group (DEX group) randomly, with 15 rats in each group. Before left anterior descending coronary artery was clamped, DEX group received dexmedetomidine with 5 mL· kg-1 body weight for 2 h (dexmedetomidine was diluted to 1μg· mL-1 with 0.9%sodium chloride injection). While I/R group and Sham group were infused 0.9%sodium chloride injection with 5 mL· kg-1 body weight for 2 h. At the end of 120 min reperfusion, the myocardial tissues were taken for determination of the infarct size and C3 expression using the Western blot method. Results:Compared with the Sham group, the infarct sizes and expressions of C3 increased obviously in the I/R group and DEX group (P< 0.05). Compared with the I/R group, the infarct sizes in DEX group were smaller and expressions of C3 were lower(P<0.05). Conclusion:Dexmedetomidine could attenuate myocardial ischemia-reperfusion injury in rats via suppressing the expression of C3.
