目的研究松果菊苷(ECH)对血管性痴呆大鼠氧化应激损伤的保护作用。方法采用间隔3d分2次结扎大鼠双侧颈总动脉法制备血管性痴呆(VD)模型;给药后,采用生化方法测定皮层及海马组织中还原型谷胱甘肽(GSH)、一氧化氮(NO)含量,谷胱甘肽过氧化物酶(GSH—Px)、一氧化氮合酶(NOS)的活力;HE染色,光学显微镜下观察各组大鼠海马组织CA1区组织结构的变化。结果与假手术组比较,模型组大鼠的皮层及海马组织中的GSH含量以及GSH-Px的活力明显下降(P〈0.01),NO含量及NOS的活力明显升高(P〈0.05,P〈0.01),海马CA1区细胞数目减少,细胞排列紊乱稀疏,细胞形态不完整,结构不正常,胞质稀少,胞核与胞质界限模糊,细胞核深染、固缩,呈三角形或不规则形,核仁不明显,并出现增生胶质细胞;与模型组比较,各给药组大鼠皮层及海马组织中的GSH含量以及GSH—Px的活力有不同程度的升高(P〈0.05,P〈0.01),NOS的活力有不同程度的降低(P〈0.05,P〈0.01),同时大鼠海马CA1区神经元排列较为整齐,结构相对正常,核固缩现象减少,深染程度降低;与阳性药组以及假手术组比较,ECH高剂量组的皮层及海马组织中GSH、NO含量,GSH—Px、NOS的活力差异均无显著性(P〉0.05),且ECH高剂量组海马CA1区神经元损伤程度低,更接近于假手术组。结论松果菊苷对血管性痴呆大鼠氧化应激损伤有较好的保护作用。
Aim To investigate the protective effects of echinacoside ( ECH ) on oxidative stress injury in vascular dementia rats. Methods Vascular dementia model was duplicated by means of permanent ligation of bilateral common carotid artery at two times intervals for three days. Biochemical methods was used to detect the GSH, NO, GSH-Px, NOS in each group rat' s cortex and hippocampus. The change of the tissue structure in CA1 area of hippocampus in each group was observed and analyzed by microscope after HE staining. Results Compared with sham group, the content of GSH and activity of GSH-Px in the rats of the model group were decreased significantly ( P 〈 0. 01 ), while the content of NO and activity of NOS were increased obviously (P 〈 0.05, P 〈 0. 01 ). Meanwhile, in tissue structure of rat' s hippocampal CA1 area, the numbers of cells were reduced, cell arrangement was sparse and in disorder, cell form was not intact and cell structure was not normal, cytoplasm, nucleus and cytoplasm were biurry, nuclei were hyperchromatic and in contraction, and were changed to triangular or irregular shape, lacking nucleoli, and proliferation of glial cells appeared. Compared with the model group, the content of GSH and activity of GSH-Px in the rats of the treatment groups were increased significantly (P 〈 0. 05, P 〈0.01 ), while the activity of NOS was decreased obviously (P 〈 0.05, P 〈 0.01 ). Meanwhile, in rat tissue structure of hippocampal CA1 area, the rat cells in each treatment group were arranged in order, the form of structure was normal, the nuclei were less hyperchromatic and contracted. Compared with Gal group and sham group, the rats of ECH high dosage group were not different in every part of experiment (P 〉0. 05). Conclusion ECH exerts protection on oxidative stress injury in vascular dementia rats.