Protective effects of aucubin against nonylphenol-induced liver toxicity by improving biochemical, inflammatory and histopathological indices

Nonylphenol (NP) is a ubiquitous environmental toxicant that is known to cause hepatotoxicity via generation of reactive oxygen species (ROS). Aucubin (AUC), an iridoid glucoside, is a potential phytochemical possessing antioxidant and anti-inflammatory features. The current study was intended to ascertain the hepatoprotective role of AUC against NP-generated liver toxicity in rats. 48 male rats were distributed into four groups. viz. Control, NP-intoxicated group (50 mg/kg), NP + AUC-treated group (50 mg/kg + 40 mg/kg) and AUC-treated group (40 mg/kg). All the doses were administered orally. Our findings indicated that the NP intoxication upregulated the alanine aminotransferase (ALT), alkaline phosphatase (ALP) and aspartate aminotransferase (AST) level. Moreover, it brought down the activities of superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), glutathione reductase (GSR) and glutathione-S-transferase (GST), as well as the glutathione (GSH) content. Conversely, the levels of malondialdehyde (MDA) and ROS were escalated. Besides, the levels of nuclear factor-kappa B (NF-κB), tumor necrosis factor-alpha (TNF-α), interleukin-1beta (IL-1β) and IL-6 as well as the cyclooxygenase-2 (COX-2) activity were elevated due to the NP administration. In addition to it, histopathological assessment displayed the prominent morphological alterations in hepatic tissues of rats. Nevertheless, treating the rats with AUC significantly (p < 0.05) abated all the NP-instigated liver damages in rats. Therefore, it was evinced that AUC could be used as a hepatoprotective agent against the NP-prompted liver toxicity owing to its antioxidant and anti-inflammatory properties.