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Can J Physiol Pharmacol. 2017 Apr;95(4):420-426. doi: 10.1139/cjpp-2016-0447. Epub 2016 Nov 1.

Sulforaphane protects against sodium valproate-induced acute liver injury.

Author information

1
a Faculty of Pharmacy, Mansoura University, Mansoura, Egypt.
2
b Faculty of Medicine, Mansoura University, Mansoura, Egypt.

Abstract

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 α 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.

KEYWORDS:

TNFα; heme oxygenase-1; hème oxygénase 1; liver injury; lésions hépatiques; sodium valproate; sulforaphane; valproate de sodium

PMID:
28112972
DOI:
10.1139/cjpp-2016-0447
[Indexed for MEDLINE]

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