Background <p>Chicoric acid (CA) has been used as a nutritional supplement, health food, and medicine because of its antioxidant property. This study aimed to investigate whether CA can prevent motor dysfunction in a zebrafish model of Parkinson’s disease (PD).</p> Methods <p>AB-strain zebrafish (24&#xa0;hours post-fertilization) were incubated with 25 µM 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) with or without CA for 5 days. The levels of malondialdehyde, glutathione, reactive oxygen species and the activities of antioxidant enzymes in brain tissue were measured. Additionally, the expression of molecules from the nuclear factor erythroid 2-related factor 2 (Nrf2) signaling pathway were assayed by Western blot.</p> Results <p>Compared with the control group, zebrafish in the MPTP group had impaired motor function. Treatment with CA prevented the changes of the total distance, the mean speed, and attenuated dopaminergic neuronal degeneration in the PD zebrafish model. CA also reduced the levels of malondialdehyde, reactive oxygen species and increased the antioxidant enzymes and glutathione level. Furthermore, CA augmented the expression of Nrf2, NQO1, HO-1, GCLC, and GCLM in the brain of the PD zebrafish model.</p> Conclusion <p>Our findings suggest the protective effects of CA may be associated with regulating the antioxidant system, possibly involving the Nrf2 signaling pathway.</p>

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Chicoric acid prevents motor dysfunction in zebrafish Parkinson’s disease model through Nrf2-mediated antioxidant effect

  • Xiaohan Zhang,
  • Mingyue Li,
  • Huilin Zhang,
  • Xin Che,
  • Guirong Zhang,
  • Bing Han

摘要

Background

Chicoric acid (CA) has been used as a nutritional supplement, health food, and medicine because of its antioxidant property. This study aimed to investigate whether CA can prevent motor dysfunction in a zebrafish model of Parkinson’s disease (PD).

Methods

AB-strain zebrafish (24 hours post-fertilization) were incubated with 25 µM 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) with or without CA for 5 days. The levels of malondialdehyde, glutathione, reactive oxygen species and the activities of antioxidant enzymes in brain tissue were measured. Additionally, the expression of molecules from the nuclear factor erythroid 2-related factor 2 (Nrf2) signaling pathway were assayed by Western blot.

Results

Compared with the control group, zebrafish in the MPTP group had impaired motor function. Treatment with CA prevented the changes of the total distance, the mean speed, and attenuated dopaminergic neuronal degeneration in the PD zebrafish model. CA also reduced the levels of malondialdehyde, reactive oxygen species and increased the antioxidant enzymes and glutathione level. Furthermore, CA augmented the expression of Nrf2, NQO1, HO-1, GCLC, and GCLM in the brain of the PD zebrafish model.

Conclusion

Our findings suggest the protective effects of CA may be associated with regulating the antioxidant system, possibly involving the Nrf2 signaling pathway.