米诺环素对帕金森病模型大鼠胶质细胞源性神经营养因子家族的影响

Minocycline affects the expression of glial cell derived neurotrophic factor family in a rat model of Parkinson’s disease

BACKGROUND:Researches have found that minocycline plays a neuroprotective effect by inhibiting the microglia cell proliferation and activation and suppressing glial cells to release cytokines and chemokines.OBJECTIVE:To investigate the influence of minocycline on glial cell line derived neurotrophic factor, NTN and gene expression in substantia nigra and corpus striatum in Parkinson’s disease model rats.METHODS:144 rats were randomly divided into four groups, with 36 rats in each group. In the normal control group, no intervention was given. In the model and experimental groups, 6-hydroxydopamine was injected in the right substantia nigra pars compacta and ventral tegmental area to establish Parkinson’s disease models. In the sham surgery group, vitamin C was injected in the two points. In the experimental group, after model establishment, rats were intragastrically given 4.5 g/L minocycline 45 mg/kg. From then on, additional 22.5 mg/kg minocycline was added every 12 hours. The last group was normal control group. Immediately, 12 hours, 1, 7, 14 and 21 days after model induction, SP immunohistochemistry was used to detect the expression of glial cell line derived neurotrophic factor and NTN expression in the substantia nigra and corpus striatum. RT-PCR was used to identify glial cell line derived neurotrophic factor and NTN mRNA expression in the substantia nigra and corpus striatum. RESULTS AND CONCLUSION:Both in the substantia nigra and corpus striatum, the positive cell number and relative gene expression of glial cell line derived neurotrophic factor and NTN were lower in the model group than in the normal control and sham surgery groups (P < 0.05). Glial cell line derived neurotrophic factor- and NTN-positive cell number and relative expression were higher in the experimental group than in the model group (P < 0.05). These findings suggest that minocycline can delay the process of Parkinson’s disease pathogenesis by promoting glial cell line derived neurotrophic factor protein and gene expression.