<p>Understanding the convoluted roles of dopamine in brain function is supreme for elucidating the pathophysiology and the therapeutic approach of movement disorders. Of which, Parkinson’s disease (PD) is a progressive neurological ailment characterized by disturbed motor and non-motor functions. Luteolin, a plant-derived flavonoid, exhibits neuroprotective properties through its antioxidant and anti-inflammatory effects. In this study, we evaluated the therapeutic potential of luteolin in a rotenone-induced Wistar rat model of PD. Results of behavior assessment showed that luteolin (25&#xa0;mg/kg and 50&#xa0;mg/kg i.p.) treatment for 28&#xa0;days significantly and dose-dependently improved motor functions. Furthermore, biochemical analysis demonstrated that luteolin restored oxidative balance by elevating glutathione (GSH) levels and reducing nitrate content. Additionally, ELISA results indicated that luteolin modulated level of tumor necrosis factor-alpha (TNF-α) and Bax, thereby reducing inflammation and neuronal apoptosis. Moreover, dopamine levels were significantly increased in rat brain homogenate, corroborating the neuroprotective effects of luteolin. Histopathological analysis further confirmed dopaminergic neuronal preservation in the cortex. These findings suggest that luteolin may serve as a potential therapeutic candidate for PD by mitigating oxidative stress, neuroinflammation, and apoptosis.</p>

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Targeting dopaminergic neuronal death: Luteolin as a therapeutic modulator in Parkinson’s disease

  • Shivani Chib,
  • Bhaskar Jyoti Dutta,
  • Gurjeet Singh,
  • Randhir Singh,
  • Shamsher Singh

摘要

Understanding the convoluted roles of dopamine in brain function is supreme for elucidating the pathophysiology and the therapeutic approach of movement disorders. Of which, Parkinson’s disease (PD) is a progressive neurological ailment characterized by disturbed motor and non-motor functions. Luteolin, a plant-derived flavonoid, exhibits neuroprotective properties through its antioxidant and anti-inflammatory effects. In this study, we evaluated the therapeutic potential of luteolin in a rotenone-induced Wistar rat model of PD. Results of behavior assessment showed that luteolin (25 mg/kg and 50 mg/kg i.p.) treatment for 28 days significantly and dose-dependently improved motor functions. Furthermore, biochemical analysis demonstrated that luteolin restored oxidative balance by elevating glutathione (GSH) levels and reducing nitrate content. Additionally, ELISA results indicated that luteolin modulated level of tumor necrosis factor-alpha (TNF-α) and Bax, thereby reducing inflammation and neuronal apoptosis. Moreover, dopamine levels were significantly increased in rat brain homogenate, corroborating the neuroprotective effects of luteolin. Histopathological analysis further confirmed dopaminergic neuronal preservation in the cortex. These findings suggest that luteolin may serve as a potential therapeutic candidate for PD by mitigating oxidative stress, neuroinflammation, and apoptosis.