论文部分内容阅读
目的:制做帕金森病“肾虚证”病证结合动物模型,通过行为学、组织病理学、生物化学指标对其进行验证,为中西医研究帕金森病在动物实验研究方面提供新的造模方法。方法:通过大鼠背部皮下长期低剂量注射鱼藤酮制造疾病模型,腹腔注射D-半乳糖造成亚急性衰老模拟肾虚证。从动物行为学、组织病理学判定疾病模型;抗氧化能力验证衰老和HPA轴功能检验肾虚证模型;补肾名方地黄饮子的干预作用,反向验证病证结合动物模型。结果:造模后大鼠的平衡、协调能力显著下降,黑质部位出现了神经细胞凋亡,与正常组比较具有统计学意义,说明帕金森疾病模型造模成功;模型组出现抗氧化能力下降显著,HPA轴功能虚性亢进明显,说明通过衰老已造成“肾虚证”证候模型;地黄饮子干预后,以上指标均有一定程度的改善,且有统计学意义。结论:帕金森病“肾虚证”病证结合动物模型造模成功。
OBJECTIVE: To establish a combined animal model of Parkinson’s disease and “kidney deficiency syndrome”, and to validate it by behavioral, histopathological and biochemical criteria to provide a new paradigm for the study of Parkinson’s disease between Chinese and Western medicine in animal experiments Modeling method. Methods: The disease model was made by injecting rotenone subcutaneously on the back of rats subcutaneously for a long time and injecting D-galactose intraperitoneally to cause subacute aging model kidney deficiency syndrome. From the animal behavior, histopathological determination of disease model; anti-oxidative capacity of aging and HPA axis function test kidney deficiency syndrome; kidney Bushen Fang Fang Di Yinzi intervention, reverse verification syndromes combined with animal models. Results: After modeling, the balance and coordination ability of rats decreased significantly, apoptosis of nerve cells appeared in substantia nigra, which was statistically significant compared with the normal group, indicating that the model of Parkinson’s disease was successfully established. The antioxidant capacity of the model group decreased Significantly, HPA axis hyperthyroidism obvious, indicating that aging has resulted in “kidney deficiency syndrome” syndrome model; Rehmanniae Yin intervention, the above indicators have a certain degree of improvement, and have statistical significance. Conclusion: Parkinson ’s disease “Kidney deficiency syndrome ” syndromes combined animal model successful.