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可乐果种子中的双黄酮类化合物可乐维酮对成年Wistar大鼠肝脏乙醇诱导的氧化应激的影响。

Effect of kolaviron, a biflavonoid complex from Garcinia kola seeds, on ethanol-induced oxidative stress in liver of adult wistar rats.

作者信息

Adaramoye O A, Awogbindin I, Okusaga J O

机构信息

Department of Biochemistry, University of Ibadan, Nigeria.

出版信息

J Med Food. 2009 Jun;12(3):584-90. doi: 10.1089/jmf.2008.0138.

Abstract

The role of oxidative stress in the pathogenesis of alcoholic diseases in the liver is well documented. Kolaviron (KV), a biflavonoid complex from Garcinia kola seeds, possesses a variety of biological activities, including antioxidant. Our aim was to investigate in vivo whether KV may attenuate oxidative stress in liver of Wistar albino rats following chronic ethanol administration. Thirty-six male Wistar albino rats were randomly divided into six groups. Toxicity was induced by administering 7.5% or 45% ethanol at 3 g/kg of body weight daily for 8 weeks. Rats were treated with KV at 200 mg/kg of body weight for the same duration. Treatment was by oral gavage. Integrity of liver was assessed by determining the levels of serum alanine and aspartate aminotransferases (ALT and AST, respectively) and alkaline phosphatase (ALP). The antioxidant status was monitored by determining the levels of hepatic superoxide dismutase (SOD), catalase (CAT), glutathione S-transferase (GST), reduced glutathione (GSH), and malondialdehyde (MDA), the end product of lipid peroxidation (LPO). Experimentally, chronic ethanol administration led to hepatotoxicity as evidenced by the increase in levels of serum ALT, AST, and ALP. Ethanol also enhanced the formation of MDA in the liver. Specifically, MDA was elevated by 70% and 98% in animals treated with 7.5% and 45% ethanol, respectively. Levels of hepatic SOD, CAT, GST, and GSH were significantly (P < .05) reduced by ethanol treatment. Co-administration of KV during ethanol treatment inhibited hepatic LPO and ameliorated SOD and GST activities. These findings demonstrated that KV could have a beneficial effect by inhibiting the oxidative damage in liver of Wistar rats caused by chronic ethanol administration.

摘要

氧化应激在酒精性肝病发病机制中的作用已得到充分证实。可乐黄酮(KV)是一种来自可乐果种子的双黄酮复合物,具有多种生物活性,包括抗氧化作用。我们的目的是在体内研究KV是否能减轻慢性给予乙醇后Wistar白化大鼠肝脏中的氧化应激。36只雄性Wistar白化大鼠被随机分为6组。通过每天以3 g/kg体重给予7.5%或45%乙醇,持续8周来诱导毒性。大鼠在相同时间段内以200 mg/kg体重接受KV治疗。通过口服灌胃给药。通过测定血清丙氨酸和天冬氨酸转氨酶(分别为ALT和AST)以及碱性磷酸酶(ALP)的水平来评估肝脏的完整性。通过测定肝脏超氧化物歧化酶(SOD)、过氧化氢酶(CAT)、谷胱甘肽S -转移酶(GST)、还原型谷胱甘肽(GSH)以及脂质过氧化(LPO)的终产物丙二醛(MDA)的水平来监测抗氧化状态。实验表明,慢性给予乙醇导致肝毒性,血清ALT、AST和ALP水平升高即为证据。乙醇还增强了肝脏中MDA的形成。具体而言,在分别用7.5%和45%乙醇处理的动物中,MDA分别升高了70%和98%。乙醇处理显著(P < .05)降低了肝脏SOD、CAT、GST和GSH的水平。在乙醇治疗期间联合给予KV可抑制肝脏LPO并改善SOD和GST活性。这些发现表明,KV通过抑制慢性给予乙醇对Wistar大鼠肝脏造成的氧化损伤可能具有有益作用。

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