Thymoquinone ameliorates renal oxidative damage and proliferative response induced by mercuric chloride in rats
Thymoquinone ameliorates renal oxidative damage and proliferative response induced by mercuric chloride in rats
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DOI：
10.1111/j.1742-7843.2008.00260.x
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发表时间：
2008-08-01
影响因子：
3.1
通讯作者：
el-Din, Osama A. Sharaf
中科院分区：
文献类型：
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作者：
Fouda, Abdel-Motaal M.;Daba, Mohamad-Hesham Y.;el-Din, Osama A. Sharaf
我们测试了百里醌（2-异丙基-5-甲基-1,4-苯醌）是否可以改善氯化汞 (HgCl2) 引起的大鼠肾脏氧化损伤和增殖反应的假设。 HgCl2 (3 mg/kg) 皮下注射给两组大鼠： (i) HgCl2-百里醌组接受百里醌（10 mg/kg/天）； (ii) HgCl2 组接受载体而不是百里醌。第三组大鼠被保留作为对照组。 HgCl2 给药后 24、48 和 72 小时处死大鼠以进行组织学和生化研究。我们的研究结果表明，用百里醌治疗可以有效防止 HgCl2 引起的肾毒性。百里醌治疗可显着改善HgCl2引起的抗氧化酶恶化、血清肌酐升高和组织学损伤。细胞凋亡和增殖反应也减少。百里醌治疗提供的最大保护在施用毒剂后48和72小时尤其明显，此时组织学损伤、肾细胞凋亡和增殖反应达到最大。这些观察结果可能部分归因于百里醌的抗氧化作用，并表明它可能是预防无机汞中毒引起的急性肾衰竭的临床上有价值的药物。
We tested the hypothesis if thymoquinone (2-isopropyl-5-methyl-1,4-benzoquinone) could ameliorate renal oxidative damage and proliferative response induced by mercuric chloride (HgCl2) in rats. HgCl2 (3 mg/kg) was administered subcutaneously to each one of two groups of rats: (i) HgCl2-thymoquinone group that received thymoquinone (10 mg/kg/day); and (ii) HgCl2 group that received vehicle instead of thymoquinone. A third group of rats was reserved as control group. Rats were killed 24, 48 and 72 hr after HgCl2 administration for histological and biochemical studies. Our findings show that treatment with thymoquinone offers imperative protection from HgCl2-induced nephrotoxicity. The deterioration of antioxidant enzymes, increment of serum creatinine and histological damage caused by HgCl2 are markedly improved by thymoquinone treatment. Apoptosis and proliferative reactions are also reduced. The maximal protection offered by thymoquinone treatment was particularly noticeable 48 and 72 hr after administration of the toxic agent at the time when histological damage, renal cell apoptosis and proliferative reactions reached their maximum. These observations may be attributed partially to the antioxidant effect of thymoquinone and suggest that it may be a clinically valuable agent in the prevention of acute renal failure caused by inorganic mercury intoxication.