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目的:探讨纳豆激酶(NK)脑保护作用的具体机制。方法:通过制备大鼠大脑中动脉阻塞(MCAO)致缺血模型,采用酶联免疫吸附实验、实时定量PCR实验、紫外分光光度法研究纳豆激酶对MCAO大鼠血小板内cAMP含量、对酪氨酸激酶1/信号转导子和转录活化子1(JAK1/STAT1)通路表达、对脑组织SOD和MDA的影响;采用荧光分光光度法检测了NK对凝血酶刺激后人刺激酶小板内钙动员动脉阻塞血小板内钙离子浓度变化。结果:NK显著增加MCAO大鼠血小板内cAMP含量,同时激活损伤部位的JAK1/STAT1通路发挥抗细胞凋亡作用,显著提升了脑组织SOD酶的活力、显著降低了MDA的含量;在体外,抑制凝血酶诱导的血小板内钙离子浓度的增加。结论:NK抗脑缺血作用的机制可能为以下几点:升高环腺苷酸含量、抑制细胞内钙释放产生抗血小板活化作用;提高机体清除自由基的能力,降低脂质过氧化物的含量而抗自由基损伤;激活JAK1/STAT1通路产生抗凋亡作用。
Objective: To investigate the specific mechanism of brain protection of Nattokinase (NK). Methods: The model of ischemia induced by middle cerebral artery occlusion (MCAO) was established in rats. Enzyme-linked immunosorbent assay (ELISA), real-time PCR and ultraviolet spectrophotometry were used to study the effect of natto kinase on the intracellular cAMP content in MCAO rats, The effect of NK expression on the activity of SOD and MDA in brain tissue after the expression of JAK1 / STAT1 pathway was detected by fluorescence spectrophotometry. Mobilization of arterial occlusion platelet intracellular calcium concentration changes. Results: NK significantly increased the cAMP content in platelets of MCAO rats and activated the JAK1 / STAT1 pathway at the injury site to exert anti-apoptotic effects, which significantly increased the activity of SOD enzyme and significantly decreased the content of MDA in MCAO rats. In vitro, Thrombin-induced increase in platelet calcium concentration. Conclusion: The mechanism of NK against cerebral ischemia may be as follows: increase the content of cyclic adenosine monophosphate, inhibit intracellular calcium release anti-platelet activation; improve the body’s ability to scavenge free radicals and reduce the lipid peroxides Content and anti-free radical damage; activate JAK1 / STAT1 pathway anti-apoptotic effect.