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Sulforaphane protects against sodium valproate-induced acute liver injury

机译:亚氟烃保护丙酸钠诱导的急性肝损伤

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摘要

Drug-induced hepatotoxicity is one of the most commonly encountered obstacles in the field of medical practice. Sodium valproate (VPA) is among many drugs with reported hepatotoxic effects. Sulforaphane (SFN) is a thiol compound found in wide abundance in cruciferous plants that has numerous reported therapeutic efficacies. The current investigation sheds light on the potential hepatoprotective effect of SFN against VPA-induced liver injury in rats. Twice daily VPA (700 mg/kg, i.p.) for 7 days induced significant biochemical alterations and hepatic histopathological damage. SFN (0.5 mg/kg, orally) for 7 days significantly boosted liver function biomarkers; it reduced serum alanine transaminase, aspartate aminotransferase, and alkaline phosphatase, and restored serum albumin concentration in a significant manner. Meanwhile, SFN significantly mitigated VPA-induced histopathological alterations. To highlight the mechanisms implicated in the observed hepatoprotective action, hepatic malondialdehyde and tumour necrosis factor alpha content significantly declined with concomitant increase in hepatic heme oxygenase-1 content and glutathione concentration with SFN treatment. In conclusion, SFN can significantly ameliorate VPA-induced hepatotoxicity and liver injury primarily by direct association between antioxidant and anti-inflammatory properties.
机译:药物诱发的肝毒性是医学实践领域最常见的障碍之一。戊二酸钠(VPA)是许多具有报告的肝毒性作用的药物中。亚氟甲烷(SFN)是一种硫醇化合物,其在红外植物中具有宽丰富,所述植物具有许多报道的治疗效果。目前调查揭示了SFN对大鼠VPA诱导的肝损伤的潜在肝保护作用。每日两次VPA(700 mg / kg,i.p.)7天诱导显着的生物化学改变和肝组织病理损伤。 SFN(0.5mg / kg,口服)7天显着提高肝功能生物标志物;它减少了血清丙氨酸转氨酶,天冬氨酸氨基转移酶和碱性磷酸酶,并以显着的方式恢复血清白蛋白浓度。同时,SFN显着减轻了VPA诱导的组织病理学改变。为了强调涉及观察到的肝保护作用的机制,肝丙二醛和肿瘤坏死因子α含量显着下降,随着肝血红素氧酶-1含量和具有SFN处理的谷胱甘肽浓度而显着下降。总之,SFN可以显着改善VPA诱导的肝毒性和肝损伤,主要通过抗氧化剂和抗炎特性之间的直接关系。

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