Objective: The objective of this study was to evaluate the neuroprotective efficacy of Betulin in MPTP-induced mice models of Parkinson’s disease (PD), focusing on its potential to mitigate mitochondrial dysfunction and oxidative stress, which are key contributors to apoptosis-mediated neuronal senescence.

Background: Parkinson’s disease (PD) is a prevalent neurodegenerative disorder characterized by the degeneration of dopaminergic (DA) neurons in the substantia nigra pars compacta. Mitochondrial dysfunction and oxidative stress are implicated in the pathogenesis of PD, leading to the activation of complex processes resulting in neuronal apoptosis. While treatments for symptomatic relief exist, a cure for PD remains elusive.

Method: In this study, Betulin’s neuroprotective effects were assessed in MPTP-induced PD rat models. Betulin, was administered to evaluate its impact on motor coordination and mitochondrial function in the midbrain of MPTP-intoxicated rats. Various parameters including mitochondrial complex activity, antioxidant enzyme levels, apoptotic protein expression, and inflammatory cytokine levels were analyzed.

Results: Betulin treatment significantly improved motor coordination in MPTP-intoxicated rats and enhanced the activity of mitochondrial complexes I, IV, and V. This was accompanied by increased levels of superoxide dismutase and mitochondrial glutathione, indicative of reduced oxidative stress. Furthermore, Betulin inhibited the expression of proapoptotic proteins like caspase-3 and Bax while promoting the expression of antiapoptotic protein Bcl-2. Betulin supplementation also led to the activation of pAkt1, which inhibited apoptosis of DA neurons. Additionally, Betulin treatment reduced the expression of proinflammatory cytokines TNF-α and IL-6, indicating its anti-inflammatory effects.

Conclusion: Betulin demonstrates promising pharmacological properties as a neuroprotective agent against MPTP-induced toxicity in PD rats. Its mechanism of action involves the phosphorylation of GSK3β via activation of Akt/ERK signaling in the mitochondrial intrinsic apoptotic pathway. These findings suggest that Betulin could serve as a potential treatment option for mitochondrial-mediated apoptotic senescence in Parkinson’s disease. Further research is warranted to validate its therapeutic potential and elucidate its molecular mechanisms in clinical settings.

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MDS Abstracts - https://www.mdsabstracts.org/abstract/neuroprotective-action-of-betulin-in-parkinsons-disease-alleviating-mitochondrial-dysfunction-and-oxidative-stress-induced-apoptosis-in-rat-model/