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机构地区:[1]南阳理工学院张仲景国医学院,南阳473004 [2]南阳医学高等专科学校,南阳473061
出 处:《科学技术与工程》2017年第12期143-146,共4页Science Technology and Engineering
基 金:国家自然科学基金(U1504826);河南省科技厅科技攻关项目(152102310224);南阳理工学院青年基金(NKKY-2016-06)资助
摘 要:观察补肾醒脑方对缺血再灌注造成损伤的血管性痴呆大鼠脑组织中My D88信号传导通路影响,探讨该方对缺血性脑损伤大鼠靶向性防治机理。成年雄性Wistar大鼠造模成功后随即等分为假手术组(A组)、模型组(B组)、吡拉西坦组(C组)、补肾醒脑方组(D组),每组12只灌胃给药。第3 d、7 d检查大鼠神经功能缺损情况,1周后检测大鼠脑组织中My D88的含量。D组神经功能缺损改善较B组改善明显(P<0.05);D组脑组织中My D88表达减少程度虽与C组比较差异不显著(P>0.05),但与B组比较差异显著(P<0.05)。补肾醒脑方能有效改善缺血再灌注造成损伤的血管性痴呆大鼠的神经损伤的症状,降低大鼠模型脑组织中信号传导转接蛋白My D88,抑制炎性反应保护大脑组织。To observe the effect of Bushen Xingnao prescription for ischemia reperfusion injury caused by MyD88 signal transduction pathway in brain tissue in vascular dementia rats, the prescription on cerebral ischemic injury in rats to target prevention mechanism was explored. The successful model of adult male Wistar rats were then divided into sham operation group ( A group) , model group ( B group) , Laci Staw group ( C group) , Bush- enxingnao prescription group (D group) , 12 rats in each group by gavage. 3 d and 7 d were examined for the neu-rological deficits of rats, and the content of MyD88 in rat brain was detected after 1 week. In D group, the neuro-logical deficits than in B group were significantly improved (P 〈0. 05) ; reduce the extent compared with C group, there was no significant difference between the expression of MyD88 in brain tissue in the D group (P 〉0. 05) , but significant difference compared with group B (P 〈0. 05). Bushen Xingnao Decoction can effectively improve vas-cular dementia caused by ischemia reperfusion injury of rat nerve damage symptoms, reduce the signal transduction in the cerebral tissues of rat models adaptor protein MyD88, inhibiting inflammatory reaction of brain protection.
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