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Background <p>Parkinson’s disease (PD) stands as the second most common neurodegenerative disease, characterized by bradykinesia, rigidity, tremors, and loss of dopaminergic neurons in the midbrain. Rotenone is a&#xa0;potential mitochondrial complex‑I inhibitor, involved in PD pathogenesis, while Cryptotanshinone (CT) exhibits neuroprotective activity by its antioxidant and anti-inflammatory properties.</p> Aim and scopes <p>This study was framed to investigate the neuroprotective potential of CT against rotenone-induced PD-like symptoms in adult zebrafish.</p> Methodology <p>Adult zebrafish (4–5&#xa0;months) were randomly divided into 6&#xa0;groups (<i>n</i> = 12), followed by placing them in separate tanks. Rotenone (5 μg/L, water exposure) and CT (10&#xa0;and 20 mg/kg, <i>i.p.</i>) were administered for 28&#xa0;days, on the basis of groups. On the 29th day, fish were sacrificed, and their brains and specific brain parts were isolated for further biochemical, neurochemical, histopathological, and immunohistochemical analysis.</p> Results <p>Results disclosed that rotenone significantly decreased locomotion and triggered anxiety-like behaviour in different mazes, while CT improved them based on the dose. Additionally, CT effectively attenuated the rotenone-induced elevated expression of neuroinflammatory markers, concurrent reduction of cytokine levels, and mitochondrial complex&#xa0;I activity. It also improved various neurotransmitter levels toward normalcy, which were generally imbalanced after rotenone administration. Moreover, the brains collected from rotenone-treated groups revealed neurodegeneration, apoptosis, and morphological alterations, whereas CT preserved neuronal integrity and morphology. Immunohistopathological analysis revealed that CT restored the expression of Nrf2, which was downregulated by rotenone, signifying neuroprotective properties.</p> Conclusion <p>This research showcased the neuroprotective potential of CT in a&#xa0;dose-dependent manner, offering an alternate therapy in PD management.</p>

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Cryptotanshinone attenuates rotenone-induced Parkinsonism in zebrafish via neurotransmitter restoration and Nrf2 activation

  • 期刊论文

  • 发表日期：

    2025年4月1日

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  • Manpreet Kaur,
  • Pratyush Porel,
  • Gaurav Singh,
  • Khadga Raj Aran

摘要

Background

Parkinson’s disease (PD) stands as the second most common neurodegenerative disease, characterized by bradykinesia, rigidity, tremors, and loss of dopaminergic neurons in the midbrain. Rotenone is a potential mitochondrial complex‑I inhibitor, involved in PD pathogenesis, while Cryptotanshinone (CT) exhibits neuroprotective activity by its antioxidant and anti-inflammatory properties.

Aim and scopes

This study was framed to investigate the neuroprotective potential of CT against rotenone-induced PD-like symptoms in adult zebrafish.

Methodology

Adult zebrafish (4–5 months) were randomly divided into 6 groups (n = 12), followed by placing them in separate tanks. Rotenone (5 μg/L, water exposure) and CT (10 and 20 mg/kg, i.p.) were administered for 28 days, on the basis of groups. On the 29th day, fish were sacrificed, and their brains and specific brain parts were isolated for further biochemical, neurochemical, histopathological, and immunohistochemical analysis.

Results

Results disclosed that rotenone significantly decreased locomotion and triggered anxiety-like behaviour in different mazes, while CT improved them based on the dose. Additionally, CT effectively attenuated the rotenone-induced elevated expression of neuroinflammatory markers, concurrent reduction of cytokine levels, and mitochondrial complex I activity. It also improved various neurotransmitter levels toward normalcy, which were generally imbalanced after rotenone administration. Moreover, the brains collected from rotenone-treated groups revealed neurodegeneration, apoptosis, and morphological alterations, whereas CT preserved neuronal integrity and morphology. Immunohistopathological analysis revealed that CT restored the expression of Nrf2, which was downregulated by rotenone, signifying neuroprotective properties.

Conclusion

This research showcased the neuroprotective potential of CT in a dose-dependent manner, offering an alternate therapy in PD management.