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目的探讨骨化三醇对多巴胺能神经元的保护作用及其可能机制。方法用骨化三醇腹腔注射治疗脂多糖(LPS)偏侧帕金森病(PD)模型大鼠。成年雄性SD大鼠60只随机分为4组1对照组:右侧黑质致密部立体定向注射2μL生理盐水;2 LPS模型组:右侧黑质致密部立体定向注射LPS 2μL(5μg·μL-1);3骨化三醇高剂量组:LPS造模前7 d和造模后14 d,分别腹腔注射骨化三醇0.1μg·kg-1;4骨化三醇低剂量组:LPS造模前7 d和造模后14 d,分别腹腔注射骨化三醇0.05μg·kg-1。每组大鼠均n=15。观察阿扑吗啡诱导的PD大鼠旋转行为变化,免疫荧光组化学法检测黑质酪氨酸羟化酶(TH)的表达,ELISA法测定黑质区炎性因子(IL-1β和TNF-α)的变化。结果骨化三醇干预组大鼠旋转圈数相对于LPS模型组明显降低,其黑质TH阳性神经元存活比率显著高于LPS模型组,且能明显减少黑质中IL-1β和TNF-α的释放量。结论骨化三醇能够减轻LPS引起的大鼠多巴胺能神经元的损害,其机制与减少免疫炎症因子的释放有关。
Objective To investigate the protective effect of calcitriol on dopaminergic neurons and its possible mechanism. Methods LPS rats were treated with intraperitoneal injection of calcitriol into Parkinson ’s disease (PD) rats. Sixty adult male Sprague-Dawley rats were randomly divided into 4 groups and 1 control group: stereotactic injection of 2 μL normal saline into the substantia nigra pars compacta; 2 LPS model group: stereotactic injection of LPS 2 μL (5 μg · μL- 1); 3 high-dose calcitriol group: LPS 7 days before modeling and 14 days after modeling, intraperitoneal injection of calcitriol 0.1μg · kg-1; 4 calcitriol low-dose group: LPS made At 7 days before model and 14 days after modeling, intraperitoneal injection of calcitriol 0.05μg · kg-1 respectively. Each group of rats n = 15. The changes of rotational behavior of apomorphine-induced PD rats were observed. The expression of tyrosine hydroxylase (TH) in substantia nigra was detected by immunofluorescence staining. The expressions of inflammatory cytokines (IL-1β and TNF-α )The change. Results Compared with LPS model group, the number of rotations in calcitriol intervention group was significantly lower than that in LPS model group. The survival rate of TH substantia nigra neurons in substantia nigra was significantly higher than that in LPS model group, and IL-1β and TNF-α The amount of release. Conclusion Calcitriol can reduce the damage of LPS-induced dopaminergic neurons in rats, and its mechanism is related to the release of immune inflammatory factors.