Ameliorative role of catechin to combat against lindane instigated liver toxicity via modulating PI3K/PIP3/Akt, Nrf-2/Keap-1, NF-κB pathway and histological profile.

Lindane (LDN) is a well-known herbicidal drug that exerts deleterious impacts on vital body organs including the liver. Catechin (CTN) is a plant-based flavonoid that demonstrates various pharmacological abilities. This trial was executed to evaluate the ameliorative efficacy of CTN to combat LDN instigated hepatotoxicity in male albino rats (Rattus norvegicus). Thirty-two rats were categorized into four groups including control, LDN (30 mg/kg), LDN (30 mg/kg) + CTN (40 mg/kg) and CTN (40 mg/kg) alone treated group. It was observed that LDN dysregulated the expressions of PI3K/PIP3/Akt and Nrf-2/Keap-1 pathway. Moreover, the activities of catalase (CAT), glutathione peroxidase (GPx), superoxide dismutase (SOD), heme‑oxygenase-1 (HO-1) and glutathione reductase (GSR) were subsided after LDN intoxication. Besides, the levels of reactive oxygen species (ROS), malondialdehyde (MDA), ALT (Alanine aminotransferase), AST (Aspartate transaminase), Gamma-glutamyl transferase (GGT) and ALP (Alkaline phosphatase) were increased whereas reduced the levels of albumin and total proteins in response to LDN exposure. Additionally, LDN administration escalated the levels of Interleukin-6 (IL-6), Nuclear factor kappa-B (NF-κB), Interleukin-1β (IL-1β), tumor necrosis factor-α (TNF-α), and the activity of cyclooxygenase-2 (COX-2). Furthermore, the gene expressions of Bcl-2-associated X protein (Bax) and Cysteinyl aspartate-acid proteases-3 (Caspase-3) were enhanced whereas the expression of B-cell lymphoma-2 (Bcl-2) was lowered following the LDN treatment. LDN instigated various histological impairments in hepatic tissues. Nonetheless, concurrent administration of CTN remarkably ameliorated liver impairments via regulating aforementioned disruptions owing to its antioxidant, anti-apoptotic and histo-protective potentials.