摘要
目的 观察1,25-二羟基维生素D3对双侧脑室内注射链脲佐菌素(ICV-STZ)诱导阿尔茨海默病(AD)模型大鼠认识功能的影响,并探讨其作用机制.方法 36只SD大鼠随机分为3组:假手术组,模型组和治疗组.Morris水迷宫测试大鼠认知功能,比色法检测各组大鼠皮质和海马丙二醛(MDA)和谷胱甘肽(GSH)含量,免疫组织化学法检测脑内cleaved-caspase-3表达.结果 Morris水迷宫测试中,与假手术组大鼠逃逸潜伏期(秒)(10.31±2.33)比较,模型组大鼠逃逸潜伏期(36.54±4.56)显著延长,(P =0.000),治疗组(26.58±2.50)比模型组潜伏期显著缩短(P=0.003).与模型组大鼠皮质和海马MDA含量(nmol/mg)[(9.81±2.23),(5.09±0.74)]比较,治疗组大鼠皮质和海马MDA含量[(6.12±1.14),(3.77±0.41)]显著减少(P=0.001,P=0.002),与模型组大鼠皮质和海马GSH含量(g/L)[(1.57 ±0.56),(1.39±0.43)]比较,治疗组大鼠皮质和海马GSH含量[(2.98±0.52),(3.05±0.78)]显著增加(P =0.005,P=0.002).免疫组织化学染色显示,与模型组皮质和海马cleavedcaspase-3阳性细胞数[(32.47±8.22),(28.58±4.32)]比较,治疗组皮质和海马阳性细胞数[(16.85±7.31),(18.12±5.64)]显著减少(P=0.021,P=0.003).结论 1,25-二羟基维生素D3能够改善STZ诱导的大鼠认知功能障碍,其机制与改善脑内氧化应激和减少神经细胞凋亡有关.
Objective To observe the effect of 1,25-dihydroxy vitamin D3 treatment on cognitive function of Alzheimer-type model rats and to investigate the mechanism.Methods 36 adult male SD rats were divided into 3 groups randomly:Sham group(s),Model group and Treatment group.The cognitive function was examined by Morris Water Maze test.The contents of malonaldehyde (MDA) and glutathione (GSH) were evaluated by the colorimetric method.Immunohistochemical method was used to assess the expression of cleavedcaspase-3.Results In Morris water maze test,compared with sham group (s) (10.31 ± 2.33),the escape latency of model group (36.54 ± 4.56) was significantly prelonged (P =0.000),compared with model group,the escape latency of treatment group (26.58 ± 2.50) was significantly shortened (P =0.003).Compared with model group(nmol/mg) [(9.81 ± 2.23),(5.09 ± 0.74)],the cortical and hippocampal MDA content of treatment group[(6.12 ± 1.14),(3.77 ± 0.41)] was decreased (P =0.001,P =0.002).Compared with model group(g/mL) [(1.57 ± 0.56),(1.39 ± 0.43)] the cortical and hippocampal GSH content of treatment group [(2.98 ± 0.52),(3.05 ± 0.78)] was increased (P =0.005,P =0.002).Compared with model group [(32.47 ± 8.22),(28.58 ± 4.32)],the expression of cortical and hippocampal cleaved-caspase-3 in treatment group [(16.85 ± 7.31),(18.12 ± 5.64)] was significantly increased (P =0.021,P =0.003).Conclusion 1,25-dihydroxy vitamin D3 treatment improved the cognitive dysfunction induced by STZ.This beneficial effect was implemented by ameliorating cerebral oxidative stress and reducing neuronal apoptosis.
出处
《国际免疫学杂志》
CAS
2016年第4期354-357,共4页
International Journal of Immunology