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龙葵提取物对四氯化碳诱导的大鼠氧化损伤的肝保护作用。

Hepatoprotective effects of Solanum nigrum Linn extract against CCl(4)-induced oxidative damage in rats.

作者信息

Lin Hui-Mei, Tseng Hsien-Chun, Wang Chau-Jong, Lin Jin-Jin, Lo Chia-Wen, Chou Fen-Pi

机构信息

Institute of Biochemistry and Biotechnology, College of Medicine, Chung Shan Medical University, Taichung, Taiwan.

出版信息

Chem Biol Interact. 2008 Feb 15;171(3):283-93. doi: 10.1016/j.cbi.2007.08.008. Epub 2007 Aug 19.

Abstract

Solanum nigrum L. (SN) is an herbal plant that has been used as hepatoprotective and anti-inflammation agent in Chinese medicine. In this study, the protective effects of water extract of SN (SNE) against liver damage were evaluated in carbon tetrachloride (CCl4)-induced chronic hepatotoxicity in rats. Sprague-Dawley (SD) rats were orally fed with SNE (0.2, 0.5, and 1.0 g kg(-1) bw) along with administration of CCl4 (20% CCl4/corn oil; 0.5 mL kg(-1) bw) for 6 weeks. The results showed that the treatment of SNE significantly lowered the CCl4-induced serum levels of hepatic enzyme markers (GOT, GPT, ALP, and total bilirubin), superoxide and hydroxyl radical. The hepatic content of GSH, and activities and expressions of SOD, GST Al, and GST Mu that were reduced by CCl4 were brought back to control levels by the supplement of SNE. Liver histopathology showed that SNE reduced the incidence of liver lesions including hepatic cells cloudy swelling, lymphocytes infiltration, hepatic necrosis, and fibrous connective tissue proliferation induced by CCl4 in rats. Therefore, the results of this study suggest that SNE could protect liver against the CCl4-induced oxidative damage in rats, and this hepatoprotective effect might be contributed to its modulation on detoxification enzymes and its antioxidant and free radical scavenger effects.

摘要

龙葵是一种草本植物,在中医中被用作保肝和抗炎药物。在本研究中,评估了龙葵水提取物(SNE)对四氯化碳(CCl4)诱导的大鼠慢性肝毒性的肝损伤保护作用。将斯普拉格-道利(SD)大鼠口服给予SNE(0.2、0.5和1.0 g kg(-1)体重),同时给予CCl4(20% CCl4/玉米油;0.5 mL kg(-1)体重),持续6周。结果表明,SNE治疗显著降低了CCl4诱导的血清肝酶标志物(谷草转氨酶、谷丙转氨酶、碱性磷酸酶和总胆红素)、超氧化物和羟自由基水平。CCl4降低的肝组织谷胱甘肽含量、超氧化物歧化酶、谷胱甘肽S-转移酶Al和谷胱甘肽S-转移酶Mu的活性及表达,通过补充SNE恢复到对照水平。肝脏组织病理学显示,SNE降低了大鼠肝脏病变的发生率,包括肝细胞浊肿、淋巴细胞浸润、肝坏死以及CCl4诱导的纤维结缔组织增生。因此,本研究结果表明,SNE可以保护肝脏免受CCl4诱导的大鼠氧化损伤,这种保肝作用可能归因于其对解毒酶的调节作用及其抗氧化和自由基清除作用。

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