Abstract
Aim:This study examines the effect of alpha-lipoic acid (ALA) on sodium valproate-induced liver injury through histological features of mice liver tissue.Materials and Methods:Mice were divided into three groups; (1) vehicle group, (2) sodium valproate group, and (3) sodium valproate-ALA group. The vehicle group was injected with saline intraperitoneal (i.p.) for 28 days. The sodium valproate group was injected with sodium valproate 300 mg/kg, i.p. daily for 2 weeks, after which the vehicle was administered daily until day 28. The sodium valproate-ALA group was injected with sodium valproate 300 mg/kg daily for 2 weeks before the administration of ALA 100 mg/kg i.p. until day 28. The mice were euthanized, and the liver was extracted for histopathological examination.Results:Histopathological examination of the liver section of the vehicle group showed a normal structure of the liver. Two weeks after the administration of sodium valproate, histopathological examination showed an abnormal structure of the liver, with necrotic appearance and inflammatory cells. Moreover, treatment with ALA after the administration of sodium valproate notably ameliorated hepatic histopathological lesions and the liver structure corresponded to a normal liver structure.Conclusion:ALA ameliorates sodium valproate-induced liver injury in mice.
Highlights
Epilepsy is one of the most common chronic neurologic disorders
Histopathological examination of the liver section of the vehicle group showed a normal structure of the liver
Two weeks after the administration of sodium valproate, histopathological examination showed an abnormal structure of the liver, with necrotic appearance and inflammatory cells
Summary
Epilepsy is one of the most common chronic neurologic disorders. 70 million people have epilepsy worldwide and approximately 90% of them are from developing regions [1]. Sodium valproate is a commonly prescribed antiepileptic drug used to treat various seizure disorders. Severe side effects such as hepatotoxicity, pancreatitis, thrombocytopenia, and platelet aggregation are associated with valproate treatment [2]. The liver is the primary organ for the metabolism of many antiepileptic drugs and is subjected to drug-induced injury. The mechanism of hepatotoxicity remains unclear, and overproduction of reactive oxygen species (ROS) and compromised antioxidant capacity as a result of oxidative stress has been hypothesized to play a role in the etiology of toxicity. Several studies have reported that valproate treatment is associated with oxidative stress [3]
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