4.5 Article

Curcumin neuroprotective effects in Parkinson disease during pregnancy

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BRAIN RESEARCH BULLETIN
卷 201, 期 -, 页码 -

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PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/j.brainresbull.2023.110726

关键词

Curcumin; Neuroprotection; Parkinson; Mice; Rotenone

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This study investigated the effects of rotenone-induced Parkinson's disease (PD) on the cerebral tissue of female mice and their fetuses, as well as the potential protective effects of curcumin supplementation. The results showed that curcumin improved cerebral cell viability by preventing cell apoptosis and necrosis in both PD mice and their fetuses. Additionally, curcumin upregulated bcl-2 expression and downregulated bax, miR-211, and circRNA 0001518 expression in cerebral neurons.
Background: Young onset Parkinson disease (YOPD) accounts for about 10% of PD patients, with the onset of symptoms between the ages of 21 and 40. At this age, the probability of pregnancy is high and there is a concern that the disease affects the fetuses. Therefore, in the present study, the effects of rotenone-induced PD on female mice as well as their fetuses and curcumin supplementation on the cerebral tissue of both female mice and their resulted fetuses were studied.Methods: The rotenone was injected subcutaneously to induce PD model of female mice. The different concentrations of curcumin were administrated every day i.p. for 3 weeks and the rotarod test was done on day 1 and 19. Cell viability was measured by MTT test and apoptosis and necrosis of cells were evaluate using flow cytometry technique. After primer design, the expressions of bax, bcl-2, miR-211 and circRNA 0001518 genes were measured using RT-PCR technique.Results: Curcumin administration were improved cerebral cell viability of both female PD mice and resulted fetuses by preventing cell apoptosis and necrosis. bax, miR-211 and circRNA 0001518 were downregulated and bcl-2 overexpressed in cerebral neurons of PD mice and their fetuses.Conclusion: PD induction in mice affects their fetal brain, and curcumin can partially reduce the negative effects of PD on fetal brain cells by overexpressing bcl-2 and decreasing bax expression genes.

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