大黄素对膳食诱导的高脂血症大鼠的血脂调节作用及其分子机制  

Regulatory Effect of Emodin on Lipid Profile in Hyperlipidemic Rats and Its Molecular Mechanism

作　　者：吴健虹 卢留珠 雷顺俊 罗媚 徐阳凤 吕纯芳 WU Jianhong;LU Liuzhu;LEI Shunjun;LUO Mei;XU Yangfeng;LV Chunfang(Shenzhen Nanshan Center for Chronic Disease Control,Shenzhen 518054,China)

机构地区：[1]深圳市南山区慢性病防治院检验科

出　　处：《激光生物学报》2019年第5期445-451,共7页Acta Laser Biology Sinica

基　　金：深圳市南山区科技创新局资助项目(2017066)

摘　　要：本研究主要对大黄素膳食诱导的高脂血症大鼠的血脂调节作用和其分子机制进行探索。SD雄性大鼠随机分为4组(每组8只):正常组、高脂血症组、辛伐他汀组和大黄素组。正常组给予正常饲料,其它组给予高脂饲料,辛伐他汀组(10 mg/kg)和大黄素组(10 mg/kg)连续灌胃给药38 d,试验结束采血测血清总胆固醇(TC)、甘油三酯(TG)、高密度脂蛋白胆固醇(HDL-C)、低密度脂蛋白胆固醇(LDL-C),比较各组的动脉粥样硬化指数(AI);肝脏做组织病理学分析;胸主动脉做体外孵育测总一氧化氮(NO),实时荧光定量PCR和免疫印迹分别测血管的内皮型一氧化氮合成酶(eNOS)的mRNA转录和蛋白表达水平。结果表明:大黄素组能够显著降低TC、TG、LDL-C(P<0.05,P<0.05,P<0.001)和AI(P<0.001)。病理学结果显示大黄素能够降低肝细胞的脂肪变性程度。胸主动脉体外培养结果显示大黄素能够显著提高总NO(P<0.05);PCR和免疫印迹结果显示大黄素能够上调eNOS的基因和蛋白水平(P<0.05,P<0.001)。因此,大黄素能够降低血清TC、TG和LDL-C,保护肝细胞,减低动脉粥样硬化发生危险;其作用的分子机制可能与上调内皮细胞eNOS/NO系统、保护血管内皮有关。To investigate the regulatory effect of emodin on lipid profile in diet-induced hyperlipidemic rats and elucidate the molecular mechanisms involved,male SD rats were randomly divided into 4 groups(8 rats for each group)including control group,hyperlipidemia group,simvastatin group and emodin group.The control group was given normal diet,and others were given diet rich in cholesterol.In the meantime,the simvastatin group and emodin group was orally administrated with simvastatin(10 mg/kg)and emodin(10 mg/kg),respectively.After continous gavage for 38 days,the lipid profile was investigated by the content of serum total cholesterol(TC),triglyceride(TG),low density lipoprotein cholesterol(LDL-C)and high density lipoprotein cholesterol(HDL-C).The atherogenic index(AI)of each group was calculated and compared.Pathological features of liver histology were observed.Thoracic aortas were isolated and divided into two sections,one for in vitro incubation and detection of total nitric oxide(NO)content in supernatant,the other for measuring the mRNA expression level of endothelial nitric oxide synthase(eNOS)by realtime fluorescence quantification PCR and the protein expression level by western blotting.The results showed that emodin markedly attenuated the increased serum TC,TG and LDL-C induced by hypercholesterolemic diet.Compared with the hyperlipidemia group,emodin significantly reduced AI value.Liver histopathology examination showed that emodin observably reduced the degree of steatosis in hepatocytes of hyperlipidemic rats.Emodin significantly increased the secretion of NO in vitro,and also upregulated both the mRNA and protein expression levels of eNOS in thoracic aortas.The results of the present experiment indicate that emodin can lower serum TC,TG,LDL-C and reduce the atherogenic properties of dietary choleaterol in rats.Its antihyperlipidemic function may be due to upregulating the level of eNOS/NO system and protecting the blood vessel endothelium.

关 键 词：大黄素 动脉粥样硬化指数 高血脂症 一氧化氮 内皮型一氧化氮合成酶 

分 类 号：R285.5[医药卫生—中药学]