CAJ | 학술논문

目的：探讨脑络通防治缺血性脑损伤的作用机制。方法：采用多因素病证结合的气虚血瘀证脑缺血动物模型。观察脑络通对血浆t-PA(tissueplasminogen activator组织型纤溶酶原激活物)、PAI(plasminogen activator inhibitor组织型纤溶酶原激活物抑制物)及血清IL-1β(interleukin-1β白细胞介素-1β)、IL-6(interleukin-6白细胞介素-6)含量的影响。结果：与缺血模型组比较，脑络通可显著提高血浆t-PA活性(p<0.01)，降低PAI活性(p<0.01)，降低血清IL-1β水平(p<0.01)及IL-6水平(p<0.05)，且优于药物对照组。结论：在脑缺血急性期，脑络通可通过改善血浆纤维蛋白溶解系统活性，调节炎性介质释放，从多个病理环节阻断缺血性脑损伤，为益气活血的中药复方制剂脑络通防治缺血性脑血管疾病提供了进一步的实验证据。
목적：탐토뇌락통방치결혈성뇌손상적작용궤제。방법：채용다인소병증결합적기허혈어증뇌결혈동물모형。관찰뇌락통대혈장t-PA(tissueplasminogen activator조직형섬용매원격활물)、PAI(plasminogen activator inhibitor조직형섬용매원격활물억제물)급혈청IL-1β(interleukin-1β백세포개소-1β)、IL-6(interleukin-6백세포개소-6)함량적영향。결과：여결혈모형조비교，뇌락통가현저제고혈장t-PA활성(p<0.01)，강저PAI활성(p<0.01)，강저혈청IL-1β수평(p<0.01)급IL-6수평(p<0.05)，차우우약물대조조。결론：재뇌결혈급성기，뇌락통가통과개선혈장섬유단백용해계통활성，조절염성개질석방，종다개병리배절조단결혈성뇌손상，위익기활혈적중약복방제제뇌락통방치결혈성뇌혈관질병제공료진일보적실험증거。
Objective: To study mechanism of NaoLuoTong on cerebral ischemicinjury. Method: Multifactorial animal model of the Qi-deficiency and blood-stasis type of cerebral ischemia was established to observe the effect of NaoLuoTong on the activity of t-PA (tissue plasminogen activator) and PAI(plasminogen activator inhibitor), the level of IL-1 β(interleukin-1 β) and IL-6(interleukin-6). Result: NaoLuoTong could remarkably increase the activity of t-PA(P<0.01)，remarkably decrease the activity of PAI(P<0.01), decrease the level of IL-1 β(P<0.01) and IL-6(P<0.05). Conclusion: NaoluoTong could improve the fibrinolytic system, reduce the excess production of inflammatory media, therefore provided a further evidence for its protective effect on ischemic cerebral injury