Background: Sodium valproate (SVP) is a widely prescribed treatment for epilepsy and other neurological diseases. However, liver injury is a harmful side effect related to its usage. Oxidative stress, inflammation, and fibrosis seem to play a major role in SVP-induced hepatotoxicity.
Aim of the work: This work aimed, for the first time, to study the possible protective mechanisms of ginger (GN) in modulating the hepatotoxic effects of SVP in albino rats.
Material and methods: A total of 24 Sprague-Dawley adult male rats (180g - 220g) were divided into equal four groups: Group1 (control): received normal saline by gavage. Group2 (GN): received ginger (200mg/kg/day). Group3 (SVP): received SVP (300mg/kg/day). Group4 (GN+SVP): received combined ginger (200mg/kg/day) and SVP (300mg/kg/day).All medications were administrated dailyfor 14 days by gavage. At the assigned time the animals were sacrificed, the blood and tissue samples were collected and processed for biochemical, histological, and immunohistochemical studies.
Result: SVP treatment induced a significant increase in alanine transaminase, aspartate transaminase, and Malondialdehyde (ALT, AST, and MDA respectively), together with a significant reduction in the antioxidant enzyme Glutathione (GHS) indicated hepatic oxidative stress damage. Histological examination revealed loss of the normal hepatic architecture, extensive fibrosis identified by Masson's trichrome staining. Moreover, the SVP group showed a significant increase in tumor necrosis factor-alpha (TNF-α) and transforming growth factor-beta (TGF-β) Immunohistochemical expression. Co-treatment with GN significantly reversed the previous changes in the GN+SVP group.
Conclusion: In conclusion, ginger has hepatoprotective activity due to its anti-oxidant, anti-inflammation, and anti-fibrotic potentials.