A therapeutic approach of LC-MS characterised MFER-Mc against alcohol and NDEA induced hepatocellular carcinoma activity through LXR-α, LXR-β and HMG-CoA pathway: an in-silico, in-vitro and in-vivo study.

Ethanol was previously classified as a co-carcinogen or tumour promoter, based on early animal studies. Ethanol may also contribute to cancer development indirectly by serving as a solvent for chemical constituents found in tobacco smoke, fried meals that contain N-nitrosodiethylamine (NDEA), led to increased production of reactive oxygen species (ROS), inflammation, fibrosis, enhanced cell proliferation, and the development of hepatocellular carcinoma (HCC). Approximately 70% of anticancer agents are derived from plant-based sources. This study was designed under in silico, in vitro, and in vivo sections, using HPTLC, LC-MS, ELISA techniques and the experiments were performed with lyophilised methanolic fruit extract residue of Morinda citrifolia (MFER-Mc) to treat alcohol and NDEA (200 mg/kg b.w., i.p.) induced HCC in Wistar albino male rats. The tyrosinase inhibitory activity observed in M. citrifolia, is associated with the lignans present, particularly 3,3'-bisdemethylpinoresinol and Americanin-A. Liver X receptors (LXRs) have recently been identified as anti-inflammatory transcription factors capable of modulating a variety of physiological processes. MFER-Mc directly interacts with molecular targets like LXR-beta, LXR-alpha, and HMG-CoA reductase to restore metabolic homeostasis and lessen carcinogenic disruptions brought on by exposure to alcohol and NDEA. To maximise benefit for patients with liver cancer and improve translation into clinical use, more research addressing pharmacokinetics, clinical efficacy, and treatment combinations is necessary.