中国药理学通报
中國藥理學通報
중국약이학통보
Chinese Pharmacological Bulletin
2015年
10期
1375-1378,1379
,共5页
朱乔燕%王光宇%毕亚光%张庆勇%魏盟
硃喬燕%王光宇%畢亞光%張慶勇%魏盟
주교연%왕광우%필아광%장경용%위맹
辛伐他汀%心肌梗死%心功能%氧化应激%急性期%p-Akt%p-eNOS
辛伐他汀%心肌梗死%心功能%氧化應激%急性期%p-Akt%p-eNOS
신벌타정%심기경사%심공능%양화응격%급성기%p-Akt%p-eNOS
simvastatin%myocardial infarction%cardi-ac function%oxidative stress%acute phase%p-Akt%p-eNOS
目的:探讨辛伐他汀( simvastatin, Sim)对急性心肌梗死后心肌内源性抗氧化系统的影响及其潜在机制。方法应用结扎大鼠冠状动脉左前降支的方法模拟急性心肌梗死( AMI),随机分为心肌梗死组( MI)组和辛伐他汀组( Sim,20 mg·kg-1·d-1),另设假手术组(Sham组)。 Sim组连续灌胃7 d,MI组和 Sham组给予等剂量的生理盐水灌胃。7 d后,观察心肌血流动力学参数变化;检测血脂及心肌坏死标记物肌钙蛋白I( c-TnI)和乳酸脱氢酶( LDH)变化;ELISA法检测心肌抗氧化系统超氧化物歧化酶( SOD)及谷胱甘肽过氧化物酶( GP )水平。 Western blot 检测心肌 p-Akt/p-eNOS蛋白表达变化。结果急性心肌梗死明显降低心肌血流动力学参数,增加血清c-TnI和LDH水平,降低SOD及GP水平,降低p-Akt和p-eNOS蛋白表达。 Sim组能明显改善急性期心功能恶化,减低血清 c-TnI 和 LDH 水平,增加 SOD 及GP水平,增加p-Akt和p-eNOS蛋白表达。结论急性心肌梗死后早期应用Sim能明显改善心功能,增加心肌抗氧化系统活性,减少心肌坏死,这可能与提高p-Akt和p-eNOS蛋白表达有关。
目的:探討辛伐他汀( simvastatin, Sim)對急性心肌梗死後心肌內源性抗氧化繫統的影響及其潛在機製。方法應用結扎大鼠冠狀動脈左前降支的方法模擬急性心肌梗死( AMI),隨機分為心肌梗死組( MI)組和辛伐他汀組( Sim,20 mg·kg-1·d-1),另設假手術組(Sham組)。 Sim組連續灌胃7 d,MI組和 Sham組給予等劑量的生理鹽水灌胃。7 d後,觀察心肌血流動力學參數變化;檢測血脂及心肌壞死標記物肌鈣蛋白I( c-TnI)和乳痠脫氫酶( LDH)變化;ELISA法檢測心肌抗氧化繫統超氧化物歧化酶( SOD)及穀胱甘肽過氧化物酶( GP )水平。 Western blot 檢測心肌 p-Akt/p-eNOS蛋白錶達變化。結果急性心肌梗死明顯降低心肌血流動力學參數,增加血清c-TnI和LDH水平,降低SOD及GP水平,降低p-Akt和p-eNOS蛋白錶達。 Sim組能明顯改善急性期心功能噁化,減低血清 c-TnI 和 LDH 水平,增加 SOD 及GP水平,增加p-Akt和p-eNOS蛋白錶達。結論急性心肌梗死後早期應用Sim能明顯改善心功能,增加心肌抗氧化繫統活性,減少心肌壞死,這可能與提高p-Akt和p-eNOS蛋白錶達有關。
목적:탐토신벌타정( simvastatin, Sim)대급성심기경사후심기내원성항양화계통적영향급기잠재궤제。방법응용결찰대서관상동맥좌전강지적방법모의급성심기경사( AMI),수궤분위심기경사조( MI)조화신벌타정조( Sim,20 mg·kg-1·d-1),령설가수술조(Sham조)。 Sim조련속관위7 d,MI조화 Sham조급여등제량적생리염수관위。7 d후,관찰심기혈류동역학삼수변화;검측혈지급심기배사표기물기개단백I( c-TnI)화유산탈경매( LDH)변화;ELISA법검측심기항양화계통초양화물기화매( SOD)급곡광감태과양화물매( GP )수평。 Western blot 검측심기 p-Akt/p-eNOS단백표체변화。결과급성심기경사명현강저심기혈류동역학삼수,증가혈청c-TnI화LDH수평,강저SOD급GP수평,강저p-Akt화p-eNOS단백표체。 Sim조능명현개선급성기심공능악화,감저혈청 c-TnI 화 LDH 수평,증가 SOD 급GP수평,증가p-Akt화p-eNOS단백표체。결론급성심기경사후조기응용Sim능명현개선심공능,증가심기항양화계통활성,감소심기배사,저가능여제고p-Akt화p-eNOS단백표체유관。
Aim To investigate the effect of simvastatin ( Sim ) on endogenous antioxidant system after acute myocardial infarction ( AMI ) and its potential mecha-nisms. Methods The acute myocardial infarction ( AMI ) rat models were made by ligation left anterior descending of coronary artery. Then the successful models were randomly divided into myocardial infarc-tion group ( MI group) and simvastatin group ( Sim,20 mg·kg-1·d-1), another group without ligation left anterior descending of coronary artery served as sham group(Sham group). The Sim group was administered simvastatin by gavage for 7 days. MI group and Sham group received saline. Hemodynamic parameters, lipid levels, troponinI ( c-TnI ) and lactate dehydrogenase ( LDH) concentrations were examined after 7days, and the levels of superoxide dismutase ( SOD) and glutathi-one peroxidase ( GP) of myocardial antioxidant system were detected by ELISA. The expression of cardiac p-Akt and p-eNOS protein were detected by Western blot. Results Acute myocardial infarction significant-ly lowered cardiac hemodynamic parameters, increased serum c-TnI and LDH levels, lowered levels of SOD and GP, and lowered the expression of p-Akt and p-eNOS protein. However, Sim could effectively prevent the deterioration of cardiac function, reduce serum c-TnI and LDH levels, increase levels of SOD and GP, and increase p-Akt and p-eNOS protein expression. Conclusion Early using Sim can effectively improve heart function after acute myocardial infarction, acti-vate myocardial antioxidant system,and reduce myocar-dial necrosis, which may be related to increasing the expression of p-Akt and p-eNOS.