Yu Zhenxiang, Xu Huali, Yu Xiaofeng, Sui Dayun, Lin Guangzhu
First Hospital of Jilin University, Changchun, 130021, PR China.
Department of Pharmacology, School of Pharmacy, Jilin University, Changchun, 130021, PR China.
Iran J Basic Med Sci. 2017 Oct;20(10):1141-1148. doi: 10.22038/IJBMS.2017.9365.
This study was to investigate the antihyperlipidemic and antioxidant effect of total flavonoid extract from (TFAK) in hyperlipidemia induced by a high-fat diet.
Male SD rats were randomly divided into 6 groups: normal group, model (hyperlipidemic diet) group, hyperlipedemic diet supplemented with TFAK (50, 100 and 200 mg/kg) and simvastatin (30 mg/kg) groups. The rats were administrated TFAK by oral for 28 days. Body weight, total cholesterol (TC), triglyceride (TG), low-density lipoprotein cholesterol (LDL-c), high-density lipoprotein cholesterol (HDL-c), superoxide dismutase (SOD), catalase(CAT), glutathione peroxidase(GSH-Px) and malondialdehyde (MDA) were measured. The atherogenic index (AI) and coronary risk index (CRI) were calculated. The activity of hydroxymethylglutaryl coenzyme A (HMG-CoA) reductase in hepatic tissue was examined. Histopathologic changes were also checked.
The levels of TC, TG and LDL-c were increased in model group. Compared to the model group, TFAK reduced significantly the body weight, TC, TG, LDL-c, AI, CRI and elevated the level of HDL-c. Moreover, the activity of SOD was elevated significantly, whereas the content of MDA decreased. The activity of HMG-CoA reductase was also decreased. Morphological evaluation found that rats in model group developed a severe steatosis, but the severity of liver steatosis was ameliorated in TFAK treated groups. The possible mechanism may be associated with decrease HMG-CoA reductase activity.
Our results suggest that TFAK exerts strong antioxidant and lipid-lowering effects, prevents hepatic fatty deposition and regulates the HMG-CoA reductase.
本研究旨在探讨朝鲜淫羊藿总黄酮提取物（TFAK）对高脂饮食诱导的高脂血症的抗高血脂和抗氧化作用。
雄性SD大鼠随机分为6组：正常组、模型（高脂饮食）组、高脂饮食补充TFAK（50、100和200mg/kg）组和辛伐他汀（30mg/kg）组。大鼠口服TFAK 28天。测量体重、总胆固醇（TC）、甘油三酯（TG）、低密度脂蛋白胆固醇（LDL-c）、高密度脂蛋白胆固醇（HDL-c）、超氧化物歧化酶（SOD）、过氧化氢酶（CAT）、谷胱甘肽过氧化物酶（GSH-Px）和丙二醛（MDA）。计算动脉粥样硬化指数（AI）和冠心病风险指数（CRI）。检测肝组织中羟甲基戊二酰辅酶A（HMG-CoA）还原酶的活性。还检查了组织病理学变化。
模型组TC、TG和LDL-c水平升高。与模型组相比，TFAK显著降低了体重、TC、TG、LDL-c、AI、CRI，并提高了HDL-c水平。此外，SOD活性显著升高，而MDA含量降低。HMG-CoA还原酶的活性也降低。形态学评估发现，模型组大鼠出现严重脂肪变性，但TFAK治疗组肝脂肪变性的严重程度有所改善。可能的机制可能与降低HMG-CoA还原酶活性有关。
我们的结果表明，TFAK具有强大的抗氧化和降脂作用，可预防肝脏脂肪沉积并调节HMG-CoA还原酶。
