基础医学与临床
基礎醫學與臨床
기출의학여림상
Basic & Clinical Medicine
2015年
1期
1-6
,共6页
决明子%糖尿病%心肌缺血/再灌注损伤%Akt%ERK1/2
決明子%糖尿病%心肌缺血/再灌註損傷%Akt%ERK1/2
결명자%당뇨병%심기결혈/재관주손상%Akt%ERK1/2
semen cassiae%diabetes%myocardial ischemia/reperfusion injury%Akt%ERK1/2
目的：研究决明子提取物（ SCE）对糖尿病大鼠心肌缺血／再灌注（ MI／R）损伤的影响。方法构建高脂饲料-链脲霉素诱导的2型糖尿病大鼠模型（HFD-STZ），大鼠随机分为对照组（Con）、SCE处理组（Con＋SCE，每日灌胃给予SCE，10 mg／kg）、糖尿病组（DM）和糖尿病SCE处理组（DM＋SCE）。1周后行心肌缺血30 min／再灌注4或6 h，并检测血浆总胆固醇（ TC）和三酰甘油（ TG）水平，用伊文氏蓝-TTC法检测心肌梗死范围、用试剂盒检测血清肌酸激酶（ CK）和乳酸脱氢酶（ LDH）活性、用TUNEL法和caspase-3试剂盒检测细胞凋亡，用Western blot 法检测Akt、ERK1／2表达及磷酸化等。结果 HFD-STZ大鼠MI／R损伤加重，虽SCE处理1周对正常动物MI／R损伤无影响，但降低HFD-STZ大鼠TC、TG水平，可将其心肌梗死面积减小至38.4％±2.7％，显著低于糖尿病组的46.1％±3.2％（ P＜0.05），且血清CK、LDH活性及细胞凋亡减少；还可增加HFD-STZ大鼠心肌Akt及ERK1／2磷酸化。用Akt或ERK1／2抑制剂可阻断SCE的心肌保护作用。结论 SCE可有效减轻糖尿病大鼠MI／R损伤，可能与其降脂并激活Akt及ERK1／2信号有关。
目的：研究決明子提取物（ SCE）對糖尿病大鼠心肌缺血／再灌註（ MI／R）損傷的影響。方法構建高脂飼料-鏈脲黴素誘導的2型糖尿病大鼠模型（HFD-STZ），大鼠隨機分為對照組（Con）、SCE處理組（Con＋SCE，每日灌胃給予SCE，10 mg／kg）、糖尿病組（DM）和糖尿病SCE處理組（DM＋SCE）。1週後行心肌缺血30 min／再灌註4或6 h，併檢測血漿總膽固醇（ TC）和三酰甘油（ TG）水平，用伊文氏藍-TTC法檢測心肌梗死範圍、用試劑盒檢測血清肌痠激酶（ CK）和乳痠脫氫酶（ LDH）活性、用TUNEL法和caspase-3試劑盒檢測細胞凋亡，用Western blot 法檢測Akt、ERK1／2錶達及燐痠化等。結果 HFD-STZ大鼠MI／R損傷加重，雖SCE處理1週對正常動物MI／R損傷無影響，但降低HFD-STZ大鼠TC、TG水平，可將其心肌梗死麵積減小至38.4％±2.7％，顯著低于糖尿病組的46.1％±3.2％（ P＜0.05），且血清CK、LDH活性及細胞凋亡減少；還可增加HFD-STZ大鼠心肌Akt及ERK1／2燐痠化。用Akt或ERK1／2抑製劑可阻斷SCE的心肌保護作用。結論 SCE可有效減輕糖尿病大鼠MI／R損傷，可能與其降脂併激活Akt及ERK1／2信號有關。
목적：연구결명자제취물（ SCE）대당뇨병대서심기결혈／재관주（ MI／R）손상적영향。방법구건고지사료-련뇨매소유도적2형당뇨병대서모형（HFD-STZ），대서수궤분위대조조（Con）、SCE처리조（Con＋SCE，매일관위급여SCE，10 mg／kg）、당뇨병조（DM）화당뇨병SCE처리조（DM＋SCE）。1주후행심기결혈30 min／재관주4혹6 h，병검측혈장총담고순（ TC）화삼선감유（ TG）수평，용이문씨람-TTC법검측심기경사범위、용시제합검측혈청기산격매（ CK）화유산탈경매（ LDH）활성、용TUNEL법화caspase-3시제합검측세포조망，용Western blot 법검측Akt、ERK1／2표체급린산화등。결과 HFD-STZ대서MI／R손상가중，수SCE처리1주대정상동물MI／R손상무영향，단강저HFD-STZ대서TC、TG수평，가장기심기경사면적감소지38.4％±2.7％，현저저우당뇨병조적46.1％±3.2％（ P＜0.05），차혈청CK、LDH활성급세포조망감소；환가증가HFD-STZ대서심기Akt급ERK1／2린산화。용Akt혹ERK1／2억제제가조단SCE적심기보호작용。결론 SCE가유효감경당뇨병대서MI／R손상，가능여기강지병격활Akt급ERK1／2신호유관。
Objective Obese patients with type 2 diabetes mellitus ( T2DM) characterized by hyperglycemia are li-able to more severe myocardial infarction .Semen Cassiae is proved to reduce serum lipid level .This study was to investigate whether the Semen Cassiae extract (SCE) reduces myocardial ischemia and reperfusion (MI/R) injury with or without diabetes and the underlying mechanisms .Methods The high-fat diet-fed streptozotocin ( HFD-STZ) rat model was used as T2DM model.Normal and DM rats received SCE treatment orally (10 mg/kg/day) for 1 week.Subsequently these animals were subjected to MI /R.Results Compared with the normal animals , DM rats showed increased plasma total cholesterol ( TC) and triacylglycerol ( TG) , more severe MI/R injury and cardi-ac functional impairment .SCE treatment significantly reduced the plasma TC and TG , improved the instantaneous first derivation of left ventricle pressure and reduced infarct size , decreased plasma creatine kinase and lactate dehydrogenase levels, and reduced apoptosis index at the end of reperfusion in diabetic rats .Moreover, SCE treat-ment increased the antiapoptotic protein Akt and stimulated ERK 1/2 phosphorylation .Pretreatment with a PI3 K in-hibitor wortmannin or an ERK1/2 inhibitor PD98059 not only blocked Akt and ERK1/2 phosphorylation, but also inhibited the cardioprotective effects of SCE .However , SCE treatment did not show any effects on the MI/R injury in the normal rats.Conclusions SCE effectively improves myocardial function and reduces MI/R-induced injury in diabetic but not normal animals , which is potentially attributable to the reduced TC/TG levels and the triggered cell survival signaling Akt and ERK 1/2 .
