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作 者:张丽霞[1] 杨清洁 ZHANG Lixia;YANG Qingjie(Department of Neurology,the Third People’s Hospital of Zhengzhou,Zhengzhou 450000,China)
机构地区:[1]郑州市第三人民医院神经内科,河南郑州450000
出 处:《河南医学研究》2025年第3期500-503,共4页Henan Medical Research
摘 要:目的基于Toll样受体4(TLR4)/核因子-κB(NF-κB)、冠状动脉微循环探讨丹参酮ⅡA治疗脑梗死的作用机制。方法采用随机数字表法将郑州市第三人民医院2023年1—4月收治的90例脑梗死患者分为对照组(45例)和观察组(45例)。对照组接受常规脑梗死治疗方法,观察组在常规脑梗死治疗方法的基础上接受丹参酮ⅡA治疗。评估两组疗效。比较两组血清抗炎因子、TLR4/NF-κB信号通路相关指标表达、冠状动脉微循环相关指标及血流量动力学参数。结果治疗后,观察组治疗总有效率、一氧化氮(NO)、管内皮生长因子(VEGF)、脑血流量(Q_(mean))、平均血流速度(V_(mean))均高于对照组(P<0.05),肿瘤坏死因子α(TNF-α)、白细胞介素-10(IL-10)、Toll样受体4(TLR4)、核因子-κB(NF-κB)、血栓素B2(TXB2)、动态阻抗(DR)、血管特征性阻抗(ZCV)、脑血管外周阻力(R)水平均低于对照组(P<0.05),两组不良反应总发生率差异无统计学意义(P>0.05)。结论丹参酮ⅡA可提高治疗脑梗死效果,其作用机制与通过调控TLR4/NF-κB信号通路降低炎症因子及改善冠状动脉微循环、血流动力参数有关,且不增加不良反应风险。Objective To investigate the mechanism of tanshinoneⅡA in treating cerebral infarction based on Toll-like receptor 4(TLR4)/nuclear factor-κB(NF-κB)and coronary microcirculation.Methods Using random number table method,90 patients with cerebral infarction admitted to the Third People’s Hospital of Zhengzhou from January to April 2023 were divided into the control group(45 cases)and the observation group(45 cases),receiving conventional treatment for cerebral infarction and tanshinoneⅡA treatment on the basis of conventional treatment,respectively.Efficacy in the two groups was evaluated.Serum anti-inflammatory factors,expression of TLR4/NF-κB signaling pathway related indexes,coronary microcirculation related indexes,and hemodynamic parameters were compared between the two groups.Results After treatment,the total effective rate of treatment,serum nitric oxide(NO)and vascular endothelial growth factor(VEGF)levels,mean blood flow(Q_(mean))and mean blood flow velocity(V_(mean))in the observation group were higher than those in the control group(P<0.05).The levels of tumor necrosis factorα(TNF-α),interleukin-10(IL-10),Toll like receptor 4(TLR4),nuclear factor kappa B(NF-κB)and thromboxane B2(TXB2),dynamic resistance(DR),vascular characteristic impedance(ZCV)and peripheral resistance(R)were lower than those in the control group(P<0.05).There was no statistically significant difference in the total incidence of adverse reactions between the two groups(P>0.05).Conclusion TanshinoneⅡA can improve the therapeutic effect on cerebral infarction.Its mechanism is related to reducing inflammatory factors and improving coronary microcirculation and hemodynamic parameters by regulating TLR4/NF-κB signaling pathway,without increasing the risk of adverse reactions.
关 键 词:脑梗死 丹参酮ⅡA TLR4/NF-κB信号通路 炎症因子 冠状动脉微循环 血流动力参数
分 类 号:R743.3[医药卫生—神经病学与精神病学]
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