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目的探讨内源性组胺在PD发病中的作用。方法采用6-羟基多巴(6-OHDA)制备偏侧毁损的PD大鼠模型,连续7 d侧脑室给予组胺合成酶抑制剂α-FMH(12.5μg,25μg)以降低脑内组胺的含量。术后第7 d观察如下指标:阿朴吗啡诱导的旋转行为;免疫组织化学法检测黑质内多巴胺能神经元和下丘脑后部结节乳头核(TMN)内组胺能神经元的免疫反应活性;高效液相色谱法检测纹状体内多巴胺的含量。结果与模型组相比,α-FMH(25μg)明显降低了阿朴吗啡诱导的PD大鼠的旋转行为(4.09与6.18 r/min相比,P<0.05);延缓了毁损侧黑质内多巴胺神经元的缺失;轻微地增加了纹状体内多巴胺的含量。此外,与假手术组相比,模型组和α-FMH给药组大鼠TMN内组胺能神经元均无明显改变。结论内源性组胺介入了PD的发病机制,但并不伴有组胺能神经元的病理改变。
Objective To investigate the role of endogenous histamine in the pathogenesis of PD. Methods 6-hydroxydopamine (6-OHDA) was used to prepare hemiparkinsonian rat models of PD. Histamine synthetase inhibitor α-FMH (12.5μg, 25μg) content. The following indexes were observed on the 7th day after surgery: apomorphine-induced rotational behavior; Immunohistochemistry was used to detect the immunoreactivity of histaminergic neurons in dopaminergic neurons in the substantia nigra and in the posterior nodular papillary nucleus (TMN) of the hypothalamus Activity; high-performance liquid chromatography to detect dopamine levels in the striatum. Results α-FMH (25 μg) significantly reduced apomorphine-induced PD rats rotation (4.09 vs. 6.18 r / min, P <0.05), delayed dopamine Deletion of neurons; slightly increased dopamine levels in the striatum. In addition, compared with the sham operation group, there was no significant change of histaminergic neurons in the TMN of the model group and the α-FMH administration group. Conclusion Endogenous histamine intervenes in the pathogenesis of PD, but not with pathological changes of histaminergic neurons.