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总序花灰木乙醇提取物对高脂血症大鼠的降血脂及抗氧化活性:氧化应激参与高脂血症的证据

Hypolipidemic and antioxidant activity of ethanolic extract of Symplocos racemosa Roxb. in hyperlipidemic rats: an evidence of participation of oxidative stress in hyperlipidemia.

作者信息

Durkar A M, Patil R R, Naik S R

出版信息

Indian J Exp Biol. 2014 Jan;52(1):36-45.

PMID:24617014
Abstract

Hypolipidemic and antioxidant activity profiles of ethanolic extracts of Symplocos racemosa (EESR) were studied by triton-WR1339 (acute) and high fat diet induced (chronic) hyperlipidemic rat models. In both the models, a significant increase in total cholesterol (TC), triglycerides (TG), very low density lipoproteins (VLDL), low density lipoproteins (LDL) and decrease in high density lipoproteins (HDL) in serum were observed. EESR (200 and 400 mg/kg) and simvastatin (10 mg/kg) administered orally reduced the elevated serum lipids (TC, TG, VLDL, LDL), restored the decreased HDL and improved the atherogenic index. In high fat diet induced hyperlipidemic model, EESR treatment prevented the increased formation of malondialdehyde (MDA) in liver, restored the depleted liver antioxidants, glutathione, superoxide dismutase, catalase significantly. The increased liver cholesterol, HMG-CoA reductase activity and body weight of hyperlipidemic rats were significantly reduced by EESR treatment. The EESR inhibited HMG-CoA reductase, a rate limiting enzyme in cholesterol biosynthesis, thereby causing hypolipidemic effects. EESR treatment also improved histoarchitecture of hepatocytes in hyperlipidemic rats. Experimental findings demonstrated anti-hyperlipidemic and antioxidant activity of EESR, which may be directly or indirectly related to its antioxidant activity. The hypolipidemic activity of EESR may be due to the presence of flavonoids phenolic compounds, phenolic glycosides and steroids.

摘要

通过 Triton-WR1339(急性)和高脂饮食诱导(慢性)的高脂血症大鼠模型,研究了灰木莲乙醇提取物(EESR)的降血脂和抗氧化活性。在这两种模型中,均观察到血清中总胆固醇(TC)、甘油三酯(TG)、极低密度脂蛋白(VLDL)、低密度脂蛋白(LDL)显著升高,高密度脂蛋白(HDL)降低。口服给予 EESR(200 和 400 mg/kg)和辛伐他汀(10 mg/kg)可降低升高的血脂(TC、TG、VLDL、LDL),恢复降低的 HDL,并改善动脉粥样硬化指数。在高脂饮食诱导的高脂血症模型中,EESR 治疗可显著预防肝脏中丙二醛(MDA)形成增加,恢复耗尽的肝脏抗氧化剂、谷胱甘肽、超氧化物歧化酶、过氧化氢酶。EESR 治疗可显著降低高脂血症大鼠肝脏胆固醇、HMG-CoA 还原酶活性和体重增加。EESR 抑制 HMG-CoA 还原酶,这是胆固醇生物合成中的限速酶,从而产生降血脂作用。EESR 治疗还改善了高脂血症大鼠肝细胞的组织结构。实验结果表明 EESR 具有抗高脂血症和抗氧化活性,这可能与其抗氧化活性直接或间接相关。EESR 的降血脂活性可能归因于黄酮类酚类化合物、酚糖苷和甾体的存在。

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