CAJ | 학술논문

目的：探讨黄芪多糖（ APS）对慢性心力衰竭（ CHF）大鼠心肌腺苷酸活化蛋白激酶（ AMPK）活性和游离脂肪酸（ FFA）代谢的影响。方法：32只雄性SD大鼠随机分为4组：正常对照组、假手术组、模型组和APS组，每组8只。采用大鼠左侧冠状动脉结扎术建立心肌梗死后心衰模型。造模成功后， APS 组大鼠给予 APS （3 g· kg－1· d－1）连续灌胃6周。采用心脏超声检测左心室舒张期内径（ LVD）、左心室收缩期内径（ LVS）、左心室射血分数（LVEF）和短轴缩短率（FS）；HE染色观察心肌病理形态学改变；乙酰辅酶A合成酶-乙酰辅酶A氧化酶法（ ACS-ACOD）检测血清及心肌FFA浓度；Western blotting法测大鼠心肌总AMPK、磷酸化AMPK（ p-AMPK）、脂肪酸转位酶（FAT／CD36）和肉毒碱软脂酰转移酶-1（CPT-1）的蛋白表达情况。结果：假手术组与对照组比较各项指标无显著差异。模型组较对照组LVEF和FS显著降低（ P＜0.05）而LVD和LVS显著增加（ P＜0.05）。 APS组LVEF和FS较模型组明显改善（P＜0.05）并且LVD和LVS较模型组明显减小（P＜0.05）。 HE染色显示模型组较对照组心肌坏死灶增加，残余心肌细胞减少；而APS组较模型组心肌坏死灶减少，残余心肌细胞增多。模型组血清及心肌FFA浓度较对照组明显增加（P＜0.05）；APS组血清及心肌FFA浓度较模型组明显减少（P＜0.05）。模型组p-AMPK、CPT-1和细胞膜FAT／CD36表达较对照组显著减少（P＜0.05）；而与模型组相比APS组p-AMPK、CPT-1和细胞膜FAT／CD36表达明显增加（ P＜0.05）。结论：APS可能通过激活慢性心衰大鼠AMPK相关通路促进心肌摄取利用FFA，从而改善慢性心衰。
목적：탐토황기다당（ APS）대만성심력쇠갈（ CHF）대서심기선감산활화단백격매（ AMPK）활성화유리지방산（ FFA）대사적영향。방법：32지웅성SD대서수궤분위4조：정상대조조、가수술조、모형조화APS조，매조8지。채용대서좌측관상동맥결찰술건립심기경사후심쇠모형。조모성공후， APS 조대서급여 APS （3 g· kg－1· d－1）련속관위6주。채용심장초성검측좌심실서장기내경（ LVD）、좌심실수축기내경（ LVS）、좌심실사혈분수（LVEF）화단축축단솔（FS）；HE염색관찰심기병리형태학개변；을선보매A합성매-을선보매A양화매법（ ACS-ACOD）검측혈청급심기FFA농도；Western blotting법측대서심기총AMPK、린산화AMPK（ p-AMPK）、지방산전위매（FAT／CD36）화육독감연지선전이매-1（CPT-1）적단백표체정황。결과：가수술조여대조조비교각항지표무현저차이。모형조교대조조LVEF화FS현저강저（ P＜0.05）이LVD화LVS현저증가（ P＜0.05）。 APS조LVEF화FS교모형조명현개선（P＜0.05）병차LVD화LVS교모형조명현감소（P＜0.05）。 HE염색현시모형조교대조조심기배사조증가，잔여심기세포감소；이APS조교모형조심기배사조감소，잔여심기세포증다。모형조혈청급심기FFA농도교대조조명현증가（P＜0.05）；APS조혈청급심기FFA농도교모형조명현감소（P＜0.05）。모형조p-AMPK、CPT-1화세포막FAT／CD36표체교대조조현저감소（P＜0.05）；이여모형조상비APS조p-AMPK、CPT-1화세포막FAT／CD36표체명현증가（ P＜0.05）。결론：APS가능통과격활만성심쇠대서AMPK상관통로촉진심기섭취이용FFA，종이개선만성심쇠。
AIM:To investigate the effect of Astragalus polysaccharides ( APS) on chronic heart failure and its mechanism.METHODS:Male SD rats (n=32) were randomly divided into control group , sham group, model group and APS group (8 rats in each group).The left coronary artery ligation in the rats was conducted to establish myocardial infarc -tion heart failure model.After modeling, the rats in APS group were given APS (3 g· kg-1· d-1) by intragastric adminis-tration for 6 weeks.Left ventricular diastolic diameter (LVD), left ventricular systolic diameter (LVS), left ventricular ejection fraction ( LVEF) and fractional shortening ( FS) were detected by echocardiography .HE staining was used to ob-serve the pathological changes .The concentrations of free fatty acid ( FFA) in the serum and myocardium were observed by the method of acetyl coenzyme A synthetase and acetyl coenzyme A oxidase ( ACS-ACOD ) .The protein levels of total AMP-activated protein kinase (AMPK), phosphorylated AMP-activated protein kinase (p-AMPK), fatty acid translocase (FAT/CD36) and carnitine palmitoyltransferase I (CPT-1) were measured by Western blotting.RESULTS: No signifi-cant difference in each index between sham group and control group was observed .Compared with control group , LVEF and FS in model group was significantly decreased , while LVD and LVS was significantly increased ( P<0.05 ) .The LVEF and FS in APS group were significantly improved compared with model group ( P<0.05 ) , and there was no significant difference between APS group and control group .LVD and LVS in APS group were obviously improved compared with mo-del group (P<0.05), and the difference was significant compared with control group (P<0.05).Compared with control group, focal myocardial necrosis increased , and residual myocardial cells reduced in model group , while those was much better in APS group as compared with model group (P<0.05).The FFA concentrations in the serum and myocardium in model group increased significantly compared with control group ( P<0.05 ) , while those decreased significantly in APS group as compared with model group (P<0.05).The protein levels of p-AMPK, CPT-1, and cell membrane FAT/CD36 in model group decreased significantly compared with control group (P<0.05), and those in APS group increased obvious-ly compared with control group (P<0.05).CONCLUSION:APS improves chronic heart failure by activating the AMPK pathway and promoting myocardial ingestion and utiliation of FFA .