Yan Sheng-lei, Yin Mei-chin
Div. of Gastroenterology, Dept. of Internal Medicine, Chang Bing Show-Chwan Memorial Hospital, Changhua County, Taiwan.
J Food Sci. 2007 Sep;72(7):S511-5. doi: 10.1111/j.1750-3841.2007.00449.x.
In vivo protective and alleviative effects of s-allyl cysteine (SAC), s-ethyl cysteine (SEC), s-methyl cysteine (SMC), and s-propyl cysteine (SPC) against alcohol-induced hepatotoxicity in Balb/cA mice were studied. In the preventive study, SAC, SEC, SMC, or SPC, each agent at 1 g/L, was added into the drinking water for 3 wk, and the mice were then treated with ethanol to induce acute liver injury. In the alleviative study, mice were first treated by ethanol followed by the 4 agent treatments for 3 wk. The preintake of these agents significantly attenuated subsequent alcohol-induced lipid oxidation, glutathione (GSH) depletion, and activity reduction of catalase and glutathione peroxidase (P < 0.05); also attenuated were the alcohol-induced elevation of c-reactive protein (CRP), interleukin-6 (IL-6), IL-10 and tumor necrosis factor (TNF)-alpha (P < 0.05). The preintake of these agents also significantly retarded alcohol-induced cytochrome P450 2E1 (CYP2E1) activity increase (P < 0.05). In the alleviative study, posttreatments from the 4 agents restored liver GSH content (P < 0.05); however, only SEC and SPC posttreatments significantly reduced lipid oxidation and alleviated the alcohol-induced elevation of CRP, IL-6, IL-10, and TNF-alpha (P < 0.05). SEC and SPC posttreatments also significantly diminished alcohol induced CYP2E1 activity (P < 0.05). These results support that SEC and SPC could provide both preventive and alleviative effects against alcohol-induced hepatotoxicity through suppression of oxidation and inflammation.
研究了S-烯丙基半胱氨酸(SAC)、S-乙基半胱氨酸(SEC)、S-甲基半胱氨酸(SMC)和S-丙基半胱氨酸(SPC)对Balb/cA小鼠酒精性肝毒性的体内保护和缓解作用。在预防研究中,将每种浓度为1 g/L的SAC、SEC、SMC或SPC添加到饮用水中,持续3周,然后用乙醇处理小鼠以诱导急性肝损伤。在缓解研究中,小鼠首先用乙醇处理,然后进行4种药物处理,持续3周。预先摄入这些药物可显著减轻随后酒精诱导的脂质氧化、谷胱甘肽(GSH)消耗以及过氧化氢酶和谷胱甘肽过氧化物酶活性降低(P<0.05);酒精诱导的C反应蛋白(CRP)、白细胞介素-6(IL-6)、IL-10和肿瘤坏死因子(TNF)-α升高也得到减轻(P<0.05)。预先摄入这些药物还显著抑制了酒精诱导的细胞色素P45酶2E1(CYP2E1)活性增加(P<0.05)。在缓解研究中,4种药物的后期处理恢复了肝脏GSH含量(P<0.05);然而,只有SEC和SPC后期处理显著降低了脂质氧化,并减轻了酒精诱导的CRP、IL-6、IL-10和TNF-α升高(P<0.05)。SEC和SPC后期处理也显著降低了酒精诱导的CYP2E1活性(P<0.05)。这些结果表明,SEC和SPC可以通过抑制氧化和炎症对酒精性肝毒性提供预防和缓解作用。