张晓娟, 郭莲军, 曲玲, 吕青. 蝙蝠葛酚性碱对大鼠局灶性脑缺血-再灌注继发炎性损伤的保护作用J. 药学学报, 2004, 39(8): 661-665.
引用本文: 张晓娟, 郭莲军, 曲玲, 吕青. 蝙蝠葛酚性碱对大鼠局灶性脑缺血-再灌注继发炎性损伤的保护作用J. 药学学报, 2004, 39(8): 661-665.
ZHANG Xiao-juan, GUO Lian-jun, QU Ling, Lü Qing. Protective effects of phenolic alkaloids from Menispermum dauricum on inflammatory injury following focal cerebral ischemia-reperfusion in ratsJ. Acta Pharmaceutica Sinica, 2004, 39(8): 661-665.
Citation: ZHANG Xiao-juan, GUO Lian-jun, QU Ling, Lü Qing. Protective effects of phenolic alkaloids from Menispermum dauricum on inflammatory injury following focal cerebral ischemia-reperfusion in ratsJ. Acta Pharmaceutica Sinica, 2004, 39(8): 661-665.

蝙蝠葛酚性碱对大鼠局灶性脑缺血-再灌注继发炎性损伤的保护作用

Protective effects of phenolic alkaloids from Menispermum dauricum on inflammatory injury following focal cerebral ischemia-reperfusion in rats

  • 摘要: 目的研究蝙蝠葛酚性碱对大鼠局灶性脑缺血-再灌注继发炎性损伤的保护作用及其机制。方法用线栓法制作大鼠右侧大脑中动脉栓塞模型,缺血2 h后,将线抽出实行再灌注,观察蝙蝠葛酚性碱对粘附分子(ICAM-1)表达、白细胞的粘附与浸润、髓过氧化物酶(MPO)活性和一氧化氮(NO)含量的影响。结果蝙蝠葛酚性碱可明显抑制ICAM-1的表达,减轻白细胞的粘附与浸润,降低缺血侧大脑皮层和海马组织中的MPO活性和NO含量。结论蝙蝠葛酚性碱对大鼠局灶性脑缺血-再灌注后的炎性损伤有明显保护作用,其机制可能与抑制ICAM-1表达,减轻白细胞的粘附与浸润,减少NO产生有关。

     

    Abstract: AimTo study the protective effects of phenolic alkaloids fromMenispermum dauricum (PAMd) on inflammatory injury following focal cerebral ischemia-reperfusion in rats. MethodsThe right middle cerebral artery of the rat was occluded by inserting a nylon suture through the internal carotid artery for 2 h, followed by reperfusion by withdrawing the suture. The expression of intercellular adhesion molecule-1 (ICAM-1) was observed by immunohistochemistry staining. The adhesiveness and infiltration of leucocytes were observed by HE staining. The activity of myeloperoxidase (MPO) and the content of nitric oxide (NO) in the cortex and hippocampus were measured. ResultsPAMd was shown to markedly inhibit ICAM-I expression, alleviate the adhesiveness and infiltration of leucocytes, and decrease the MPO activity and the NO content in ischemic cortex and hippocampus. ConclusionPAMd has protective effects on inflammatory injury following focal cerebral ischemia-reperfusion by inhibiting ICAM-I expression, alleviating the adhesiveness and infiltration of leucocytes and decreasing the generation of NO.

     

/

返回文章
返回