Journal of Pharmacognosy & Natural Products

In local Indian and Chinese medicine, the plant is used to treat a variety of ailments. In ayurvedic medicine, it is used to treat chronic cough, insomnia, epilepsy, hallucinations, anxiety, and other conditions. There will be more opportunities for future research and development on the herb pluricaulis as a result of the comprehensive review of the plant profile, pharmacognosy, phytochemistry, and toxicological data. Electronic searches (using PubMed, SciFinder, Google Scholar, and Web of Science) and library searches for articles published in peer-reviewed journals were used to gather information. Additionally, some local books on ethnopharmacology provided information. The majority of the pharmacological that has been used for a long time in ayurvedic, traditional Chinese, and other indigenous medical systems to treat liver disease, epileptic disease, microbial disease, cytotoxic and viral diseases, and central nervous system (CNS) disease. CNS depression, anxiolytic, tranquilizing, antidepressant, antistress, neurodegenerative, antiamnesic, antioxidant, hypolipidemic, immunomodulatory, analgesic, antifungal, antibacterial, antidiabetic, antiulcer, anticatatonic, and cardiovascular activity are among the many pharmacological effects of the crude extract and isolated metabolites.

In clinical settings, PPAR (peroxisome proliferator-activated receptor gamma) agonists are utilized to combat hyperglycemia. The search for new PPAR activators, on the other hand, is fueled by the experience of undesirable side effects like weight gain. We utilized a mix of in silico, in vitro, cell-based and in vivo models to distinguish and approve regular items as promising leads for halfway original PPARγ agonists. It was predicted in silico that the natural product honokiol from the traditional Chinese medicine Magnolia bark would bind as a dimer into the PPAR ligand binding pocket. In fact, in a PPAR-mediated luciferase reporter assay, Honokiol acted as a partial agonist by binding directly to the purified LBD of PPAR. After that, the effects of Honokiol on adipogenic differentiation in 3T3-L1 pre-adipocytes and mouse embryonic fibroblasts and the stimulation of glucose uptake in adipocytes were directly compared to those of the full agonist pioglitazone, which is currently in use in clinical settings. Unlike pioglitazone, which induced adipogenesis, honokiol did not stimulate basal glucose uptake to the same extent as pioglitazone did. The oral administration of honokiol slowed weight gain and prevented hyperglycemia in diabetic KKAy mice. In vivo, we found that honokiol was a partial non-adipogenic PPAR agonist that stopped hyperglycemia and weight gain.