Neurotrophic effect magnolol on MPTP/p induced parkinsons disease by regulation of PI3K-AKT-GSK3β via MAPK/mTOR signalling pathway

Introduction Parkinson's disease (PD) dopaminergic loss may be slowed down by neurotrophic factors (NTFs) activating at a higher level by regulating several signalling pathways, including PI3K, AKT, and Ras-MAPK. Therefore, the goal of the current investigation is to ascertain how neurotrophic magnolol (ML) is about the neurotoxicity of MPTP/p in Parkinson's disease. Methods Five weeks of ML treatment markedly reduced the motor impairments, decrease in tyrosine kinase receptor expression (TrKB) and dopamine deficiency and NTFs caused by MPTP/p. Results Additionally discovered that ML treatment markedly reduced the activation of MAPK/P38/JNK-related proteins. Additionally, ML therapy enhanced phosphorylation of PI3K, Akt, GSK-3β, and mTOR, indicating ML regulated the PI3K/Akt/mTOR signaling pathway, this reason ML has protected the Brain system. In a chronic parkinson's disease, the current study provides more comprehensive in vivo evidence supporting the neuroprotective action of ML on dopaminergic neurons. Conclusion It also raises the idea of employing ML as a novel chemotherapeutic medication.