Kinsenoside alleviates MPTP-induced Parkinson's disease via Akt activation and apoptosis inhibition in a mouse model.

Parkinson's disease (PD) is a common neurodegenerative disorder primarily characterized by motor dysfunction; however, recent studies have highlighted a broad spectrum of non-motor symptoms, including cognitive impairment and psychological harm. While dopaminergic drugs effectively manage motor symptoms in the early stages, efficacy often declines, and symptoms may worsen as the disease progresses. Kinsenoside, the primary bioactive compound from Anoectochilus formosanus, exhibits diverse pharmacological effects, yet its potential in treating PD remains unexplored. This study evaluated whether Kinsenoside could alleviate PD symptoms in a mouse model induced by 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP). Behavioral results demonstrated that Kinsenoside significantly attenuated bradykinesia in the pole test, reduced motor deficits in the traction test, and enhanced long-term cognitive memory in the passive avoidance test. Furthermore, Kinsenoside treatment significantly restored dopamine (DA) levels and increased tyrosine hydroxylase (TH) expression in the substantia nigra of PD mice. Mechanistically, Kinsenoside activated the Akt signaling pathway and decreased the protein expression ratio of Bcl-2-associated X protein (Bax) to B-cell lymphoma 2 (Bcl-2), thereby inhibiting neuronal apoptosis. These findings suggest that Kinsenoside exerts potent neuroprotective effects and represents a promising therapeutic candidate for alleviating both motor and non-motor symptoms associated with Parkinson's disease.