Abstract

To analyze the protective effect and mechanism of beta-asarone from Acorus tatarinowii on neuron injury in rats with Parkinson's disease. Thirty five male Sprague Dawley rats were randomly selected to establish the rat model of Parkinson's disease. The rats were divided into 5 groups as sham operation group, model group, low dose beta-asarone group, medium dose beta-asarone group and high dose betaasarone group, with 7 rats in each group. Rats in the sham operation group and model group were injected with the same amount of normal saline, while rats in the low dose group, middle dose group and high dose group were injected with 10 mg/kg, 20 mg/kg and 40 mg/kg beta-asarone respectively. The behavior and the expression of tyrosine hydroxylase, alpha-synuclein, superoxide dismutase, catalase, glutathione peroxidase, interleukin-1 beta, interleukin-6, tumor necrosis factor-alpha, B-cell lymphoma 2-associated X protein, B-cell lymphoma 2 and caspase-3 in brain tissue were detected level detection. Compared with the sham operation group, the number of autonomic activities, roll down time, forelimb activity time, the expression levels of alpha-synuclein, superoxide dismutase, catalase, glutathione peroxidase and B-cell lymphoma 2 were significantly decreased and the expression levels of tyrosine hydroxylase, interleukin-1 beta, tumor necrosis factor-alpha, nitric oxide, interleukin-6, B-cell lymphoma 2-associated X protein and caspase-3 were significantly increased in the model group (p<0.05) The expression levels of alphasynuclein, superoxide dismutase, catalase, glutathione peroxidase and B-cell lymphoma 2 were significantly decreased, while the expression levels of tyrosine hydroxylase, interleukin-1 beta, tumor necrosis factoralpha, nitric oxide, interleukin-6, B-cell lymphoma 2-associated X protein and caspase-3 were significantly increased (p<0.05). Low dose of beta-asarone may inhibit oxidative stress and inflammatory reaction, inhibit cell apoptosis, inhibit the decrease of tyrosine hydroxylase expression and the overexpression of alpha-synuclein, so as to play a certain neuroprotective role and reduce neuron damage.