Objective: To evaluate the therapeutic potential of baicalein and to investigate its underlying neuroprotective mechanism in a rotenone-induced mouse model of Parkinson’s disease.

Background: Parkinson’s disease (PD) is a progressive neurodegenerative disorder characterized by oxidative stress, α-synuclein aggregation, mitochondrial dysfunction, and loss of dopaminergic neurons. Reduced levels of neurotrophic factors, particularly brain-derived neurotrophic factor (BDNF), play a critical role in PD progression. Rotenone, a pesticide that inhibits mitochondrial complex I, induces excessive reactive oxygen species (ROS) production, leading to oxidative damage and α-synuclein accumulation. The BDNF–TrkB signaling pathway activates downstream kinases such as Akt and glycogen synthase kinase-3β (GSK-3β), which regulate neuronal survival and development. Additionally, the transcription factor CREB controls BDNF gene expression, and disruption of these pathways is closely associated with the progression of PD.

Method: A rotenone-induced Parkinson’s disease mouse model was used to assess the neuroprotective effects of baicalein. Baicalein, a bioactive flavone isolated from Scutellaria baicalensis Georgi, was administered at an optimized dose of 200 mg/kg body weight. Behavioral and molecular analyses were performed to examine motor function and the involvement of signaling pathways associated with neuronal survival, including CREB, Akt, and GSK-3β phosphorylation.

Results: Treatment with baicalein significantly improved motor dysfunction in rotenone-induced PD mice. The compound enhanced CREB-mediated regulation and increased the phosphorylation of Akt and GSK-3β, suggesting activation of neuroprotective signaling pathways. These findings indicate that baicalein alleviates oxidative stress-related neuronal damage and modulates key molecular pathways associated with neuronal survival.

Conclusion: The present study demonstrates that baicalein exhibits significant neuroprotective effects in a rotenone-induced mouse model of Parkinson’s disease. The protective effects are likely mediated through modulation of the BDNF/CREB/Akt signaling pathway, suggesting that baicalein may serve as a promising therapeutic agent for the treatment of Parkinson’s disease.

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MDS Abstracts - https://www.mdsabstracts.org/abstract/baicalein-attenuates-rotenone-induced-neurodegeneration-by-regulating-bdnf-creb-akt-signaling-in-parkinsons-disease/