Gymnema sylvestre as a potential therapeutic agent for PCOS: insights from mRNA differential gene expression and molecular docking analysis

Abstract

Abstract Background In spite of the increased prevalence of Polycystic Ovary Syndrome in bilateral ovaries (PCOS) in females globally (~ 20%), the rate of decisive treatment is limited due to late and invasive diagnostics and the unavailability of stand-alone drugs against phenotypic symptoms associated with PCOS. This study aims at unravelling molecular mechanisms allied with this disorder and identifying genes and pathways that are altered causing PCOS as a pre-requisite need. Furthermore, this study intends at assessing the therapeutic potentials of Gymnemasylvestre phytocompounds mainly triterpene saponins against targeted proteins and helps in seeking exemplar drug candidates. The study is designed in 2 major parts—firstly identifying key proteins involved in pathophysiology by tracing back the deregulated genes in mRNA expression profiles of PCOS Patients obtained from GEO datasets database further compared and analysed by GEO2R Analyzer and significantly deregulated genes were subjected to PPI network, KEGG and GO analysis using STRING and ShinyGO tools. The second half of the study involved molecular docking its visualisation and in silico pharmacological analysis of imminent phytocompounds revealing plausible drug candidates. Results In the study, most implied deregulated genes were MRP gene family, ICT1, NDUFA12, VDAC3, APOO, TOMM5, COX6C, COX7B, EDN1 and EDN3 genes whose functional enrichment suggests flawed metabolism of proteins and damaged mitochondrial translation. With high binding affinity, less toxicity at higher dose level Lupeol, Beta-Amyrin, Beta-Elemene, Stigmasterol, Gymnestrogenin and Dammarane proves to be efficient drug candidates. Conclusion The findings of this study imply better understanding of the molecular mechanism of the disorder and encourage further clinical studies pertaining to medicinal natural phytocompounds of Gymnemasylvestre.