Aluminium-Induced Hepatotoxicity and the Protective Role of Withania somnifera (Ashwagandha) in Wistar Rats

Aluminium is a widely distributed environmental contaminant whose chronic exposure leads to accumulation in multiple organs, including the liver, resulting in oxidative stress and tissue damage. When reactive oxygen species production exceeds the body's antioxidant defense capacity, cellular injury ensues — a mechanism central to aluminium-induced hepatotoxicity. Withania somnifera (Ashwagandha), an evergreen herb of the Solanaceae family widely cultivated in India, has been reported to exert diverse pharmacological effects, including antioxidant, anti-inflammatory, and hepatoprotective activities. This study aimed to evaluate the protective potential of Withania somnifera against aluminium chloride (AlCl₃)-induced hepatic damage in Wistar rats. Twenty-four healthy male Wistar rats (150–200 g) were randomly divided into four groups (n = 6 per group): control, Ashwagandha-treated, AlCl₃-intoxicated, and AlCl₃-intoxicated pretreated with Ashwagandha. All treatments were administered for three weeks. Hepatic oxidative stress was assessed by measuring malondialdehyde (MDA) and glutathione (GSH) levels in tissue homogenates. Serum alanine aminotransferase (SGPT/ALT) and aspartate aminotransferase (SGOT/AST) were analyzed as markers of hepatic function. Histopathological examination of liver tissue was also performed. AlCl₃ administration significantly reduced hepatic GSH content and elevated MDA, SGPT, and SGOT levels relative to controls, alongside marked histopathological alterations. Pretreatment with Ashwagandha significantly restored GSH levels, reduced MDA, and normalized SGPT and SGOT, with corresponding improvement in liver histology. These findings demonstrate that Withania somnifera effectively mitigates aluminium-induced hepatotoxicity, likely through its antioxidant mechanisms, supporting its potential as a hepatoprotective agent in aluminium-exposed populations.