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S-烯丙基半胱氨酸和S-乙基半胱氨酸对蛋氨酸胆碱缺乏饮食诱导的小鼠肝毒性的缓解作用。

Alleviative effects of s-allyl cysteine and s-ethyl cysteine on MCD diet-induced hepatotoxicity in mice.

作者信息

Lin Chun-che, Yin Mei-chin, Liu Wen-hu

机构信息

Department of Internal Medicine, Chung Shan Medical University Hospital, Taichung City, Taiwan, ROC.

出版信息

Food Chem Toxicol. 2008 Nov;46(11):3401-6. doi: 10.1016/j.fct.2008.08.010. Epub 2008 Aug 20.

Abstract

Alleviative effects of s-allyl cysteine (SAC) and s-ethyl cysteine (SEC) upon methionine and choline deficient (MCD) diet-induced hepatotoxicity in mice were examined. SAC or SEC at 1g/L was added into drinking water for 7 weeks with MCD diet. MCD feeding significantly increased hepatic triglyceride and cholesterol levels, and elevated the activity of glucose-6-phosphate dehydrogenase (G6PDH), malic enzyme, fatty acid synthase (FAS) and 3-hydroxy-3-methylglutaryl coenzyme A reductase (P < 0.05). However, the intake of SAC or SEC significantly decreased hepatic triglyceride accumulation, and reduced G6PDH and FAS activities (P < 0.05). MCD feeding significantly lowered serum and hepatic glutathione (GSH) levels, increased malondialdehyde (MDA) and oxidized glutathione (GSSG) formation, and suppressed the activity and mRNA expression of glutathione peroxidase (GPX), superoxide dismutase (SOD) and catalase (P < 0.05). The intake of SAC or SEC significantly increased serum and hepatic GSH levels, decreased MDA and GSSG formation, restored the activity and mRNA expression of GPX, SOD and catalase (P < 0.05). MCD feeding significantly enhanced the mRNA expression of interleukin (IL)-1beta, IL-6, tumor necrosis factor (TNF)-alpha, transforming growth factor (TGF)-beta1, matrix metalloproteinases-9 (MMP-9) and collagen-alpha1 (P < 0.05). The intake of SAC and SEC significantly blunted the mRNA expression of IL-1beta, IL-6, TNF-alpha, TGF-beta1 and collagen-alpha1 (P < 0.05). SEC was greater than SAC in suppressing IL-6 and TNF-alpha expression (P < 0.05), but SAC was greater than SEC in suppressing collagen-alpha1 and TGF-beta1 expression (P < 0.05). These data suggest that SAC and SEC are potent agents against MCD-induced hepatotoxicity.

摘要

研究了S-烯丙基半胱氨酸(SAC)和S-乙基半胱氨酸(SEC)对蛋氨酸和胆碱缺乏(MCD)饮食诱导的小鼠肝毒性的缓解作用。将1g/L的SAC或SEC添加到饮水中,与MCD饮食一起给予小鼠7周。给予MCD饮食显著增加了肝脏甘油三酯和胆固醇水平,并提高了葡萄糖-6-磷酸脱氢酶(G6PDH)、苹果酸酶、脂肪酸合酶(FAS)和3-羟基-3-甲基戊二酰辅酶A还原酶的活性(P<0.05)。然而,摄入SAC或SEC显著降低了肝脏甘油三酯的积累,并降低了G6PDH和FAS的活性(P<0.05)。给予MCD饮食显著降低了血清和肝脏谷胱甘肽(GSH)水平,增加了丙二醛(MDA)和氧化型谷胱甘肽(GSSG)的形成,并抑制了谷胱甘肽过氧化物酶(GPX)、超氧化物歧化酶(SOD)和过氧化氢酶的活性及mRNA表达(P<0.05)。摄入SAC或SEC显著增加了血清和肝脏GSH水平,降低了MDA和GSSG的形成,恢复了GPX、SOD和过氧化氢酶的活性及mRNA表达(P<0.05)。给予MCD饮食显著增强了白细胞介素(IL)-1β、IL-6、肿瘤坏死因子(TNF)-α、转化生长因子(TGF)-β1、基质金属蛋白酶-9(MMP-9)和胶原蛋白-α1的mRNA表达(P<0.05)。摄入SAC和SEC显著抑制了IL-1β、IL-6、TNF-α、TGF-β1和胶原蛋白-α1的mRNA表达(P<0.05)。在抑制IL-6和TNF-α表达方面,SEC大于SAC(P<0.05),但在抑制胶原蛋白-α1和TGF-β1表达方面,SAC大于SEC(P<0.05)。这些数据表明,SAC和SEC是对抗MCD诱导的肝毒性的有效药物。

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