Objective: This study aimed to investigate the neuroprotective potential of emodin in a rotenone-induced PD model and to elucidate its underlying molecular mechanisms focusing on the SIRT1/NLRP3 signaling axis and Nrf2-mediated antioxidant responses.

Background: Parkinson’s disease (PD) is a progressive neurodegenerative disorder characterized by selective degeneration of dopaminergic neurons in the Substantia Nigra Pars Compacta, resulting in motor impairment and neuroinflammation. Mitochondrial dysfunction, oxidative stress, and inflammasome activation are key mechanisms involved in PD pathogenesis. Emodin, a naturally occurring anthraquinone derivative, has demonstrated promising pharmacological activities including antioxidant, anti-inflammatory, and mitochondrial protective effects.

Method: Experimental Parkinson’s disease was induced by repeated administration of Rotenone, followed by treatment with Emodin for 18 days. Motor performance was assessed using rotarod and pole tests. Brain tissues were analyzed for oxidative stress markers, antioxidant proteins including Heme Oxygenase-1, and inflammatory mediators. Dopaminergic neuronal integrity was evaluated by immunostaining of Tyrosine Hydroxylase, and molecular docking was performed with Monoamine Oxidase B.

Results: Emodin treatment significantly improved motor performance and restored striatal dopamine levels in rotenone-treated animals. It suppressed the expression of NLRP3 and NF-κB while upregulating SIRT1, indicating modulation of the SIRT1/NF-κB/NLRP3 signaling axis. Emodin also enhanced Nrf2-mediated antioxidant responses, increasing Heme Oxygenase-1 and glutathione levels while reducing lipid peroxidation. Histological analysis showed increased Tyrosine Hydroxylase-positive neurons and reduced neurodegeneration in the substantia nigra, hippocampus, and cerebral cortex. Additionally, emodin decreased apoptotic signaling marked by reduced Caspase-3 activation.

Conclusion: Emodin exerts significant neuroprotective effects against rotenone-induced Parkinsonian neurodegeneration by attenuating oxidative stress, regulating SIRT1/NLRP3-mediated neuroinflammation, and enhancing Nrf2-dependent antioxidant defenses. These findings highlight emodin as a promising therapeutic candidate for mitigating neurodegeneration associated with Parkinson’s disease.

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MDS Abstracts - https://www.mdsabstracts.org/abstract/neuroprotective-effects-of-emodin-against-rotenone-induced-parkinsonism-through-regulation-of-sirt1-mediated-inflammasome-and-nrf2-pathways/