Abstract
Background: Parkinson’s disease is a progressive nervous system disorder caused by a degenerative loss of dopaminergic neurons of midbrain, from the substantia nigra to the corpus striatum pathway. Quercetin has a neuroprotective effect to prevent the greater loss of substantia nigra dopaminergic neurons in Parkinson’s disease model. Objectives: This study aimed to investigate the effect of the flavonoid quercetin on the behavioral test in 1-methyl-4-phenyl,2,3,6-tetrahydropyridine(MPTP)-induced male NMRI mice. Methods: Animals were divided into eight groups (n = 12). Behavioral tests of bar test and treatment with quercetin began one day after inducing the disease and lasted for 35 days. Then, brains were excluded from craniums for histology, immunohistochemistry tyrosine hydroxylase, measurement of TNF-α levels, and gene expression of caspase 3. Results: Data showed that orally taking quercetin for 35 days improved the behavioral test of bar tests in Parkinson’s disease. Cell density in TH staining was counted and showed considerable decreases in the substantia nigra in Parkinson’s disease group (83.67 ± 12.811) while it was higher in quercetin-treated groups PD + Q1 (103.67 ± 8.090) and PD + Q2 (145.33 ± 13.908) than in Parkinson’s disease group (P < 0.05). Quercetin decreased inflammation due to MPTP in the substantia nigra in PD + Q1 (1395.73 ± 1.058) and PD + Q2 (1250.66 ± 1.95), and corpus striatum in PD + Q1 (1207.033 ± 2.228) and PD + Q2 (1187.44 ± 1.64) and TNF-α protein levels in the quercetin-treated group (P < 0.05). Parkinson’s disease decreased gene expression of caspase 3 (0.35 ± 0.019) and increased it in quercetin-treated groups PD + Q1 (1.26 ± 0.062) and PD+Q2 (2.27 ± 0.144) (P < 0.0001). Conclusions: Quercetin is a natural flavonoid with neuroprotection effect and antioxidant, anti-inflammatory, and anti-apoptosis properties preventing the loss of dopaminergic neurons in mice with Parkinson’s disease.
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