Modulation of neuroinflammation by inulin and magnesium in a rotenone-induced Parkinson’s disease model | ||
| Egyptian Pharmaceutical Journal | ||
| Articles in Press, Corrected Proof, Available Online from 10 March 2025 PDF (927.38 K) | ||
| DOI: 10.21608/epj.2025.416645 | ||
| Abstract | ||
| Background Neuroinflammation is a recognized mechanism in the development and pathogenesis of Parkinson’s disease (PD). Chronic pesticide exposure has been linked to neuroinflammation and neuronal loss. Emerging evidence suggests that targeting inflammatory pathways through natural compounds and dietary interventions may help manage PD symptoms. Objective This study aims to elucidate the effects of inulin and/or magnesium supplementation on rotenone-induced PD in mice. Materials and methods Sixty Swiss adult male mice (10-13 weeks old) weighing 25±5 g were used. They were divided into healthy and Parkinson's disease groups, the latter was further subdivided into 5 groups: control-PD, PD treated with Sinemet, PD supplemented with inulin, PD supplemented with magnesium, and PD supplemented with both inulin and magnesium. Biochemical assessments of oxidative stress, inflammation, apoptosis, and mitochondrial dysfunction were conducted, along with evaluations of intestinal short-chain fatty acids and microscopic examination of brain tissue. Results and conclusion Data were analyzed using the statistical package for the social sciences (SPSS) version 16.0 for microsoft windows, provided by SPSS Inc. The obtained results showed that rotenone injection significantly altered brain function and structure, inducingneuro-oxidative stress, neuroinflammation, and apoptosis. This was markedly alleviated by individual supplementation with either inulin or magnesium, while combined supplementation showed less improvement. Thus, individual oral supplementation with inulin or magnesium could enhance the gut-brain axis and offer neuroprotection against PD progression in mice, while the combination is less preferred. | ||
| Keywords | ||
| Parkinson’s disease; neuroinflammation; inulin; magnesium; rotenone; oxidative stress; apoptosis; mitochondrial dysfunction; gut-brain axis; neuroprotection | ||
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