大蒜和洋葱中的有机硫化合物二烯丙基二硫醚可减轻三氯甲烷诱导的大鼠肝脏氧化应激、NFkB激活和细胞凋亡

Oluwatobi T. Somade, Regina N. Ugbaja, Adetunji A. Alli, Omolola T. Odubote, Taiwo S. Yusuf, Babatosin T. Busari
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引用次数: 12

摘要

三氯甲烷(TCM)是农药配方和灭火器的一种成分。据报道,它是一种肝和肾毒素。因此,我们研究了二烯丙基二硫醚(DADS)对中药肝毒性的化学预防作用。25只大鼠被分成5组,每组5只。口服中药200 mg/kg,同时联合DADS(50 mg/kg)治疗,每周5天,连用3周。与对照组相比,核因子κ B (NFkB)、TUNEL阳性细胞(凋亡)的肝脏表达以及丙二醛(MDA)、过氧化氢(H2O2)和一氧化氮(NO)的浓度均显著升高。此外,在中药治疗后,p53的表达、过氧化氢酶(CAT)和谷胱甘肽过氧化物酶(GPx)的活性以及还原型谷胱甘肽(GSH)的水平均显著降低。治疗后,与中药组相比,DADS干预显著降低了肝脏NFkB表达、凋亡阳性细胞以及MDA、H2O2、NO水平,显著提高了GSH水平、CAT和GPx活性,对p53表达的影响不显著。因此,DADS对中药诱导的肝毒性的保护作用可能是通过抑制大鼠NFkB激活、细胞凋亡和氧化应激来实现的。
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Diallyl disulfide, an organo-sulfur compound in garlic and onion attenuates trichloromethane-induced hepatic oxidative stress, activation of NFkB and apoptosis in rats

Trichloromethane (TCM) serves as an ingredient in pesticide formulations and fire extinguishers. It is a reported hepato- and renal-toxin. We therefore investigated the chemo-preventive effect of diallyl disulfide (DADS) on TCM-induced hepatotoxicity. Twenty five rats, divided into five groups of five animals each were used. TCM at the dose of 200 mg/kg was orally administered, and concomitantly treated with DADS (50 mg/kg), 5 days per week for 3 weeks. Compared with control, there was a significant increase in hepatic expressions of nuclear factor kappa B (NFkB), TUNEL positive cells (apoptosis), and concentrations of malondialdehyde (MDA), hydrogen peroxide (H2O2), and nitric oxide (NO). Also, a significant decrease in expressions of p53, and activities of catalase (CAT) and glutathione peroxidase (GPx), as well as level of reduced glutathione (GSH) was recorded following TCM administration. Following treatment, DADS intervention significantly reduced the hepatic NFkB expressions, apoptotic positive cells as well as levels of MDA, H2O2, and NO, and also significantly increased the level of GSH, activities of CAT and GPx compared with TCM group, while its effect on expressions of p53 was insignificant. Hepato-protection by DADS against TCM-induced hepatotoxicity may therefore be via suppressions of NFkB activation, apoptosis, and oxidative stress in rats.

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