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目的我们前期研究证实6-羟基多巴胺(6-OHDA)明显诱导性帕金森病(PD)模型大鼠行为学障碍及其纹状体神经元的损伤。目前进一步借助褪黑素(MT)探查证实6-羟基多巴胺对PD模型大鼠纹状体代谢机能损害和黑质DA能神经元的保护作用。方法选取55只成年雄性SD大鼠,并随机分成正常对照组(包括正常对照和稀释剂对照)、6-OHDA处理组和6-OHDA+MT处理组,实验借助Micro PET-CT、免疫组织化学染色及Westernblot技术检测和比较实验大鼠纹状体代谢、TH阳性纤维密度及TH蛋白表达量的变化。所获得数据使用SPSS20.0统计学软件进行分析处理,P<0.05为有统计学意义。结果 Micro PET-CT检测结果显示,6-OHDA组大鼠纹状体糖代谢机能(1.34±0.114)明显较对照组(4.36±0.114)低(P=0.00),而6-OHDA+MT处理组(4.14±0.114)与6-OHDA组相比糖代谢机能增高,差异也具有统计学意义(P=0.00)。纹状体内TH阳性纤维密度和TH蛋白表达水平在6-OHDA组(分别为0.324±0.018、0.434±0.338)均显著低于对照组(0.378±0.026、1.626±0.526)(P=0.00,P=0.00)和6-OHDA+MT处理组(0.37±0.010、1.136±0.494)(P=0.00,P=0.03),但对照组和6-OHDA+MT处理组之间差异无统计学意义(P=0.52,P=0.12)。结论褪黑素对PD模型大鼠纹状体代谢机能障碍和中脑黑质DA能神经元损伤具有一定的保护作用。
Purpose Our previous study demonstrated that behavioral disorders and striatal neuronal damage in 6-hydroxydopamine (6-OHDA) -induced Parkinson’s disease (PD) model rats. At present, further investigation of melatonin (MT) is used to confirm the protective effect of 6-hydroxydopamine on striatum metabolism and substantia nigra DA neurons in PD model rats. Methods Fifty-five adult male Sprague-Dawley rats were randomly divided into normal control group (including normal control and diluent control), 6-OHDA group and 6-OHDA + MT group. Micro PET-CT, immunohistochemistry The changes of striatum metabolism, TH positive fiber density and TH protein expression were detected and compared by Western blotting and Western blotting. The data obtained using SPSS20.0 statistical software analysis and processing, P <0.05 was considered statistically significant. Results Micro PET-CT showed that the function of glycometabolism in striatum of 6-OHDA group (1.34 ± 0.114) was significantly lower than that of control group (4.36 ± 0.114) (P = 0.00) (4.14 ± 0.114) Compared with the 6-OHDA group, the glucose metabolism increased, the difference was also statistically significant (P = 0.00). The TH-positive fiber density and TH protein expression in striatum were significantly lower in the 6-OHDA group (0.324 ± 0.018, 0.434 ± 0.338, respectively) than those in the control group (0.378 ± 0.026 and 1.626 ± 0.526, P = 0.00, P = (P = 0.00, P = 0.03), but there was no significant difference between the control group and the 6-OHDA + MT treatment group (P = 0.00) and the 6-OHDA + MT treatment group (0.37 ± 0.010,1.136 ± 0.494) 0.52, P = 0.12). Conclusion Melatonin has some protective effects on the metabolic dysfunction of striatum and DA neurons in substantia nigra of PD model rats.