Neuroprotective Effects of Resveratrol on a Mouse Model of Parkinson's Disease via the Wnt/Beta-Catenin Signaling Pathway

Abstract

We herein aimed to evaluate the neuroprotective effects of resveratrol on a mouse model of Parkinson’s disease and to explore whether the Wnt/beta-catenin signaling pathway was involved. Thirty male C57 black 6 mice were randomly divided into a control group, a model group (1-methyl-4-phenyl-1,2,3,6- tetrahydropyridine) and a treatment group (1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine resveratrol) (n=10). The model and treatment groups were intraperitoneally injected with 1-methyl-4-phenyl-1,2,3,6- tetrahydropyridine (30 mg/kg in normal saline) to induce Parkinson’s disease. Then the treatment group was administered with resveratrol (20 mg/kg in 0.5 % sodium carboxymethylcellulose solution) on the 1st d of modeling. The motor coordination ability was studied by the pole climbing test. Astrocyte and microglia activations in the substantia nigra pars compacta were observed by immunohistochemical staining. 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine-induced striatum dopamine release was measured by high performance liquid chromatography and dopamine transporter level was detected with Western blot. SH-SY5Y cell viability and dependence on the Wnt/beta-catenin signaling pathway were assessed by 3-(4,5-dimethylthiazolyl-2)-2,5-diphenyltetrazolium bromide assay and Western blot, respectively. Resveratrol relieved the motor dysfunction, death of dopaminergic neurons, activation of astrocytes and microglia, as well as reduction of striatum dopamine content induced by neurotoxin 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine in vitro. It also alleviated the damage of SH-SY5Y cells induced by 1-methyl- 4-phenylpyridinium. Resveratrol increased the levels of proteins from the Wnt/beta-catenin signaling pathway in the mouse model of Parkinson’s disease and 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine- treated SH-Y5Y cells. Resveratrol exerted neuroprotective effects on the Parkinson’s disease model predominantly by regulating the Wnt/beta-catenin signaling pathway.