Baicalin increases connexin 43 expression in striatal astrocytes of rats with Parkinson’s disease / 中国组织工程研究

ABSTRACT

BACKGROUND: In the pathogenesis of Parkinson’s disease, connexin 43 is an important regulatory protein, and the underlying mechanism of connexin 43 in reducing the damage of dopamine neurons is still unclear. Baicalin has been shown to inhibit the inflammation and oxidative stress of Parkinson’s disease, and can protect dopamine neurons from deformation in a rat model of Parkinson’s disease. OBJECTIVE: To investigate the effect of baicalin on the behavior and the expression of connexin 43 in astrocytes in a rat model of Parkinson’s disease. METHODS: Eighty Sprague-Dawley rats were enrolled. Ten randomly selected rats received no intervention (control group), and Parkinson’s disease was induced by unilateral bisite (median substantia nigra, striatum) lesions using 6-hydroxydopamine stereotaxic apparatus in the remaining rats. The model rats received the treatment of normal saline (model group), 125 mg/kg Madopar, 50 and 100 mg/kg baicalin, respectively, for 28 consecutive days. The changes in rotational behavior were observed by behavioral tests. The number of cells positive for tyrosine hydroxylase was determined by immunohistochemistry. The expression of connexin 43 was detected by immunohistochemistry and western blot assay. RESULTS AND CONCLUSION: Behavioral results: there was no rotational behavior in the control group before and after intervention. In the other four groups, the model group rats exhibited rotational behaviors at 5 minutes after apomorphine injection, all were at a speed of 13 r/min before treatment (P ＞ 0.05). Compared with the model group, the number of rotations in the Madopar and high-dose baicalin groups was significantly decreased (P ＜ 0.01). There was no significant difference in the number of cells positive for tyrosine hydroxylase in the nigra between model and low-dose baicalin groups (P ＞ 0.05). The number of cells positive for tyrosine hydroxylase in the Madopar and high-dose baicalin groups was significantly greater than that in the model group (P ＜ 0.01). There was a significant increase in the expression of connexin 43 in the model group compared with the control group (P ＜ 0.01). The expression level did not differ significantly between model and low-dose baicalin groups (P ＞ 0.05). The expression level in the Madopar and high-dose baicalin groups was significantly lower than that in the model group (P ＜ 0.01). In conclusion, 100 mg/kg baicalin can significantly improve the rotational behavior of rats with Parkinson’s disease, significantly increase the number of tyrosine hydrogenase-positive cells, and alleviate the damage of Parkinson’s disease neurons caused by 6-hydroxydopamine. Additionally, baicalin can down-regulate connexin 43 expression in astrocytes of rats with Parkinson’s disease.