Neuromodulatory potential of Asparagus racemosus and its bioactive molecule Shatavarin IV by enhancing synaptic acetylcholine level and nAChR activity

Cholinergic dysfunction has been commonly known to be associated with plethora of neurodegenerative disorders and also serves as a biomarker. Recently, cholinergic system demonstrated that acetylcholine has major role in regulation of its function therefore the main therapeutic regimens towards disease management have been focused on increasing acetylcholine levels. The current study explores the potential of Asparagus racemosus extract (ARE) and its bioactive molecule Shatavarin IV (SIV) in improving cholinergic transmission via utilizing Caenorhabditis elegans considering as a model system. Observations and results obtained through this study have clearly showed significant modulation in cholinergic function by increasing acetylcholine (ACh) levels and the nicotinic acetylcholine receptors (nAChRs) activity. Further exploration on mechanistic facet pointed towards ARE and SIV modulatory potential through increased synaptic ACh level by blocking acetyl cholinesterase at enzyme level and by regulating increment in transcript level of cha-1, and cho-1 that are directly responsible for the synthesis of ACh. Further, the up-regulation of unc-38 and unc-50 transcripts could be the reason for enhanced nAChR activity and investigation on stress modulator activity showed excellent efficiency of ARE and SIV in diminishing ROS thereby lowering the oxidative damage.

Automated summary

The study explores the potential of Asparagus racemosus extract (ARE) and its bioactive molecule Shatavarin IV (SIV) in improving cholinergic transmission, showing significant modulation in cholinergic function through increasing acetylcholine levels and nicotinic acetylcholine receptors activity. Further investigations suggest that ARE and SIV modulate synaptic ACh levels by blocking acetyl cholinesterase and regulating the synthesis of ACh, resulting in enhanced nAChR activity and lowering oxidative damage by diminishing ROS.