CAJ | 학술논문

目的：探讨黄芪多糖（astragalus polysaccharides ，APS）对游离脂肪酸（free fatty acid ，FFA ）导致的大鼠胰岛β细胞脂毒性的保护作用及机制。方法体外分离培养Wistar大鼠胰岛细胞，分为4组：对照组、APS组、FFA组、FFA＋APS组。各组细胞培养72 h测胰岛内三酰甘油（TG）、游离脂肪酸（FFA）含量，基础状态胰岛分泌情况，Western blot法测胰岛β细胞内总腺苷酸活化蛋白激酶（A M PK ），磷酸化腺苷酸活化蛋白激酶（p-A M PK ），肉毒碱软脂酰转移酶-1（CPT-1）、乙酰辅酶A羧化酶（ACC）的蛋白表达情况。结果①FFA使胰岛内 TG、FFA含量增加（均 P＜0.01），APS使胰岛内TG、FFA含量减少（均 P＜0.01）；②油红O染色提示FFA组胰岛内脂质蓄积增加，APS可减少脂质蓄积；③FFA使胰岛素分泌增加（P＜0.01），APS减少胰岛素分泌（P＜0.01）；④FFA抑制p-AMPK、CPT-1、ACC表达，APS使p-AM PK、CPT-1、ACC表达增加（均 P＜0.01）。结论 FFA使胰岛内脂质蓄积增加，胰岛素分泌增加，形成高胰岛素血症。APS可以通过AMPK脂代谢途径减少胰岛内脂质蓄积，同时减少胰岛素分泌，减轻高胰岛素血症，从而对 FFA导致的大鼠胰岛β细胞脂毒性起到保护作用。
목적：탐토황기다당（astragalus polysaccharides ，APS）대유리지방산（free fatty acid ，FFA ）도치적대서이도β세포지독성적보호작용급궤제。방법체외분리배양Wistar대서이도세포，분위4조：대조조、APS조、FFA조、FFA＋APS조。각조세포배양72 h측이도내삼선감유（TG）、유리지방산（FFA）함량，기출상태이도분비정황，Western blot법측이도β세포내총선감산활화단백격매（A M PK ），린산화선감산활화단백격매（p-A M PK ），육독감연지선전이매-1（CPT-1）、을선보매A최화매（ACC）적단백표체정황。결과①FFA사이도내 TG、FFA함량증가（균 P＜0.01），APS사이도내TG、FFA함량감소（균 P＜0.01）；②유홍O염색제시FFA조이도내지질축적증가，APS가감소지질축적；③FFA사이도소분비증가（P＜0.01），APS감소이도소분비（P＜0.01）；④FFA억제p-AMPK、CPT-1、ACC표체，APS사p-AM PK、CPT-1、ACC표체증가（균 P＜0.01）。결론 FFA사이도내지질축적증가，이도소분비증가，형성고이도소혈증。APS가이통과AMPK지대사도경감소이도내지질축적，동시감소이도소분비，감경고이도소혈증，종이대 FFA도치적대서이도β세포지독성기도보호작용。
Objective To investigate the protective effect of astragalus polysaccharides (APS) on the lipotoxicity of free fatty acid (FFA) to islet βcells and its mechanism.Methods Pancreatic islet cells of Wistar rat were isolated and cultured in vitro.They were divided into four groups :control group ,APS group ,FFA group ,FFA +APS group.The content of triglycer-ides (TG) and FFA and the insulin secretion were measured in cells cultured for 72 h in each group.The expression of total AM P-activated protein kinase (AM PK ) ,phosphorylated adenylate-activated protein kinase (p-AM PK ) ,carnitine palmitoyl transferase-1 (CPT-1) ,acetyl CoA carboxylase(ACC) were detected by Western blot.Results ①The contents of TG and free fatty acid were increased in the FFA group (P<0.01) but decreased in the FFA+APS group (P <0.01);②Oil Red O stai-ning showed that lipid accumulation increased in the FFA group but reduced in the FFA +APS group(P<0.01);③FFA could increase the insulin secretion (P< 0.01) ,and APS could reduce the insulin secretion (P< 0.01). ④ The expressions of p-AMPK ,CPT-1 and ACC were significantly inhibited in the FFA group but conspicuously increased in the FFA +APS group (P<0.01).Conclusion FFA can increase lipid accumulation and insulin secretion in the islets and lead to hyperinsulinemia.APS can reduce lipid accumulation and insulin secretion in the islets and alleviate hyperinsulinemia through AM PK-mediated lipid metabolism pathway ,and it can protect islet βcells against FFA-caused lipotoxicity.