Muhammad Umar Ijaz¹, Rabia Azmat¹, Derya Karataş Yeni², Asma Ashraf^3,, Vanitha Mariappan^4,

Cisplatin (CP), a widely used chemotherapeutic drug for cancer treatment is associated with multiple toxicities that limit its clinical application. Pogostemon cablin (Blanco) Benth contains pachypodol, a flavonoid with tremendous bioactive properties. The recent study intended to determine the mitigative role of pachypodol against cisplatin-instigated hepatic damage in albino rats. In this research, 32 albino rats were segregated into four groups (n = 8/group) and treated for 28 consecutive days; 1st group was designed as control, rats of the 2nd group received 10 mg/kg of CP; rats of the 3rd group were co-administered with 10 mg/kg of CP + 20 mg/kg of pachypodol, and 4th group rats received 20 mg/kg of pachypodol. Our results disclosed that CP exposure resulted in a substantial decrease in the activities of antioxidant enzymes i.e., catalase (CAT), glutathione peroxidase (GPx), superoxide dismutase (SOD), glutathione reductase (GSR), glutathione (GSH), and glutathione S-transferase (GST) as well as a notable rise in malondialdehyde (MDA) and reactive oxygen species (ROS) levels. CP exposure escalated levels of nuclear factor kappa B (NF-κB), interleukin-1β (IL-1β), tumour necrosis factor-alpha (TNF-α), interleukin-6 (IL-6) and cyclooxygenase-2 (COX-2) activity. Conversely, it diminished anti-apoptotic protein (Bcl-2) levels and elevated pro-apoptotic markers (Bax, caspase-9 and caspase-3). Besides, histopathological analysis revealed evident morphological alterations in the rats' livers. However, pachypodol significantly abated all the liver damage prompted by CP in rats. Taken together, our findings suggested that pachypodol alleviated cisplatin-induced hepatic impairment by inhibiting oxidative stress, inflammation and apoptosis.

Pachypodol, Oxidative stress, Hepatotoxicity, Cisplatin