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S-烯丙半胱氨酸通过调节 NF-κB 的表达缓解铬(VI)诱导的大鼠肝毒性中的炎症。

S-Allyl cysteine alleviates inflammation by modulating the expression of NF-κB during chromium (VI)-induced hepatotoxicity in rats.

机构信息

1 Biochemistry and Biotechnology Laboratory, Central Leather Research Institute, Council of Scientific and Industrial Research (CSIR), Adyar, Chennai, India.

2 Cell Biology Laboratory, Department of Biochemistry, University of Madras, Guindy Campus, Chennai, India.

出版信息

Hum Exp Toxicol. 2017 Nov;36(11):1186-1200. doi: 10.1177/0960327116680275. Epub 2016 Dec 15.

Abstract

Hexavalent chromium (Cr (VI)) is a common environmental pollutant. Cr (VI) exposure can lead to severe damage to the liver, but the preventive measures to diminish Cr (VI)-induced hepatotoxicity need further study. S-allyl cysteine (SAC) is a constituent of garlic ( Allium sativum) and has many beneficial effects to humans and rodents. In this study, we intended to analyze the mechanistic role of SAC during Cr (VI)-induced hepatotoxicity. Male Wistar albino rats were induced with 17 mg/kg body weight to damage the liver. The Cr (VI)-induced rats were treated with 100 mg/kg body weight of SAC as an optimum dosage to treat hepatotoxicity. We observed that the levels of oxidants, lipid peroxidation and hydroxyl radical (OH) were increased, and enzymatic antioxidants such as superoxide dismutase, catalase, glutathione peroxidase, and glutathione reductase were found to be decreased in Cr (VI)-induced rats. While treated with SAC, the levels of oxidants were decreased and enzymatic antioxidants were significantly ( p < 0.05) increased. Lysosomal enzyme activities were increased in Cr (VI)-induced rats and on treatment with SAC, the activities were significantly decreased. The expressions of nuclear factor-kappa B (p65-NF-κB), tumor necrosis factor α (TNF-α), and inducible nitric oxide synthase (iNOS) were increased during induction with Cr (VI). Subsequent administration of SAC to animals showed a decrease in the expressions of NF-κB, TNF-α, and iNOS. Results obtained from this study clearly demonstrated that SAC protects the liver cells from the Cr (VI)-induced free radical damage.

摘要

六价铬(Cr(VI))是一种常见的环境污染物。Cr(VI)暴露会导致肝脏严重损伤,但减少 Cr(VI)诱导的肝毒性的预防措施仍需要进一步研究。S-烯丙基半胱氨酸(SAC)是大蒜(Allium sativum)的一种成分,对人类和啮齿动物有许多有益的影响。在这项研究中,我们旨在分析 SAC 在 Cr(VI)诱导的肝毒性中的作用机制。雄性 Wistar 白化大鼠用 17mg/kg 体重诱导肝损伤。用 100mg/kg 体重的 SAC 处理 Cr(VI)诱导的大鼠,作为治疗肝毒性的最佳剂量。我们观察到,Cr(VI)诱导的大鼠中氧化剂、脂质过氧化和羟基自由基(OH)的水平升高,超氧化物歧化酶、过氧化氢酶、谷胱甘肽过氧化物酶和谷胱甘肽还原酶等酶抗氧化剂的水平降低。用 SAC 处理后,氧化剂水平降低,酶抗氧化剂水平显著升高(p<0.05)。Cr(VI)诱导的大鼠溶酶体酶活性升高,用 SAC 处理后,酶活性显著降低。核因子-κB(p65-NF-κB)、肿瘤坏死因子α(TNF-α)和诱导型一氧化氮合酶(iNOS)的表达在 Cr(VI)诱导时增加。随后用 SAC 处理动物,NF-κB、TNF-α和 iNOS 的表达减少。这项研究的结果清楚地表明,SAC 可以保护肝细胞免受 Cr(VI)诱导的自由基损伤。

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