西部中医药
西部中醫藥
서부중의약
GANSU JOURNAL OF TRADITIONAL CHINESE MEDICINE
2013年
9期
23-25
,共3页
消栓通络胶囊%脑缺血再灌注%TNF-α%IL-1β%实验研究
消栓通絡膠囊%腦缺血再灌註%TNF-α%IL-1β%實驗研究
소전통락효낭%뇌결혈재관주%TNF-α%IL-1β%실험연구
XiaoShuang TongLuo capsule%cerebral ischemia-reperfusion%TNF-α%IL-1β%experimental study
目的：观察消栓通络胶囊对急性缺血性中风模型大鼠脑组织肿瘤坏死因子-α(TNF-α)和白介素-1β(IL-1β)水平的影响，以探讨其治疗缺血性中风的作用机制。方法：采用线栓法制备大鼠大脑中动脉缺血再灌注(MCAO)模型，测定大鼠脑组织中TNF-α和IL-1β的水平。结果：与模型组比较，消栓通络胶囊大、中(1.68、0.84 g/kg)剂量组可明显降低MCAO大鼠神经行为学评分(P＜0.01)，可明显降低MCAO大鼠患侧脑匀浆中TNF-α和IL-1β的水平(P＜0.01)。结论：消栓通络胶囊可提高急性脑缺血再灌注大鼠的神经功能活动能力，其治疗缺血性中风的作用机制可能与TNF-α和IL-1β的表达有关。
目的：觀察消栓通絡膠囊對急性缺血性中風模型大鼠腦組織腫瘤壞死因子-α(TNF-α)和白介素-1β(IL-1β)水平的影響，以探討其治療缺血性中風的作用機製。方法：採用線栓法製備大鼠大腦中動脈缺血再灌註(MCAO)模型，測定大鼠腦組織中TNF-α和IL-1β的水平。結果：與模型組比較，消栓通絡膠囊大、中(1.68、0.84 g/kg)劑量組可明顯降低MCAO大鼠神經行為學評分(P＜0.01)，可明顯降低MCAO大鼠患側腦勻漿中TNF-α和IL-1β的水平(P＜0.01)。結論：消栓通絡膠囊可提高急性腦缺血再灌註大鼠的神經功能活動能力，其治療缺血性中風的作用機製可能與TNF-α和IL-1β的錶達有關。
목적：관찰소전통락효낭대급성결혈성중풍모형대서뇌조직종류배사인자-α(TNF-α)화백개소-1β(IL-1β)수평적영향，이탐토기치료결혈성중풍적작용궤제。방법：채용선전법제비대서대뇌중동맥결혈재관주(MCAO)모형，측정대서뇌조직중TNF-α화IL-1β적수평。결과：여모형조비교，소전통락효낭대、중(1.68、0.84 g/kg)제량조가명현강저MCAO대서신경행위학평분(P＜0.01)，가명현강저MCAO대서환측뇌균장중TNF-α화IL-1β적수평(P＜0.01)。결론：소전통락효낭가제고급성뇌결혈재관주대서적신경공능활동능력，기치료결혈성중풍적작용궤제가능여TNF-α화IL-1β적표체유관。
Objective:To discuss the mechanism of XiaoShuang TongLuo capsule in treating ischemic stroke through observing the effects of the drugs on TNF-αand IL-1βof cerebral tissue of rats with acute ischemic stroke. Method:Rat models with middle cerebral artery occlusion (MCAO) were established, the levels of TNF-αand IL-1βin cerebral tissue were detected. Result: Compared with the model group, high and middle dosage group of Xi-aoShuang TongLuo capsule (1.68 and 0.84g/kg) could obviously decrease the scales of neurological behavior of MA-CO rats remarkably (P<0.01), and lower the levels of TNF-αand IL-1βin cerebral homogenate of the affected side in MACO rat (P<0.01). Conclusion:XiaoShuang TongLuo capsule could improve the performance and neurological function of the rats with acute cerebral ischemia-reperfusion injury, its mechanism might be related to the expres-sions of TNF-αand IL-1β.
