摘要
目的 基于Toll样受体4(TLR4)核因子-κB(NF-κB)通路-神经相关因子探究依达拉奉对急性脑梗死(ACI)患者炎症反应与神经损伤的保护机制.方法 选取2020-07-2023-07保定市第一中心医院收治的110例ACI患者,以随机数字表法分为观察组、对照组,各55例,对照组给予阿替普酶溶栓,观察组给予阿替普酶溶栓联合依达拉奉治疗.比较2组疗效、神经功能[美国国立卫生研究院卒中量表(NIHSS)评分、改良Rankin评分]、TLR4 NF-κB通路指标(TLR4、NF-κB)、神经损伤相关因子[神经元特异性烯醇化酶(NSE)、中枢神经特异性蛋白(S-100β)、脑源性神经营养因子(BDNF)]、TLR4 NF-κB通路相关炎症因子[白介素-1β(IL-1β)、超敏C反应蛋白(hs-CRP)、肿瘤坏死因子(TNF-α)、五聚素3(PTX3)、脂蛋白相关磷脂酶A2(Lp-PLA2)].结果 观察组总有效率96.36％,高于对照组的83.64％(P＜0.05).治疗1、2周观察组NIHSS评分、改良Rankin评分均低于对照组(P＜0.05),观察组TLR4、NF-κB均低于对照组(P＜0.05).相较于治疗前,2组治疗1、2周后S-100β、NSE水平明显下降,BDNF水平明显升高,观察组S-100β、NSE水平均低于对照组,BDNF水平高于对照组(P＜0.05).相较于治疗前,2组治疗1、2周后IL-1 β、hs-CRP、TNF-α、PTX3、Lp-PLA2 水平均明显下降,观察组 IL-1β、hs-CRP、TNF-α、PTX3、Lp-PLA2 水平均低于对照组(P＜0.05).结论 依达拉奉对ACI患者的疗效显著,有利于缓解炎症反应,改善神经损伤,其保护机制可能与TLR4 NF-κB通路调控神经损伤、炎症反应相关因子有关.
Abstract
Objective To investigate the protective mechanism of edaravone on inflammatory response and neurological injury in acute cerebral infarction(ACI)patients based on Toll-like receptor 4(TLR4)nuclear factor kappa B(NF-κB)pathway and neurocorrelation factor.Methods A total of 110 patients with ACI admitted to Baoding First Central Hospital from July 2020 to July 2023 were selected and were randomly divided into the observation group and the control group by random number table method,with 55 cases in each group.The control group was given alteplase thrombolysis,while the observation group was given alteplase thrombolysis combined with edaravone.The efficacy,neurological function(NIHSS score,modified Rankin scale score),TLR4 NF-κB pathway indicators(TLR4,NF-κB),nerve injury related factors[neuron specific enolase(NSE),central nervous system specific protein(S-100β),brain derived neurotrophic factor(BDNF)],and TLR4 NF-κB pathway related inflammatory factors[interleukin-1 β(IL-1[3),high sensitivity C-reactive protein(hs-CRP),tumor necrosis factor(TNF-α),pentraxin 3(PTX3),lipoprotein associated phospholipase A2(Lp-PLA2)]were compared between the two groups.Results The total effective rate of the observation group was 96.36％,which was higher than 83.64％in the control group(P＜0.05).The NIHSS score and modified Rankin scale score in the observation group after 1 week and 2 weeks of treatment were lower than those in the control group(P＜0.05).The TLR4 and NF-κB levels in the observation group were lower than those in the control group after 1 week and 2 weeks of treatment(P＜0.05).Compared to before treatment,S-100 β and NSE in both groups decreased significantly after 1 week and 2 weeks of treatment,while BDNF increased significantly.Furthermore,the observation group had lower levels of S-100β and NSE than the control group,but higher levels of BDNF(P＜0.05).Compared to before treatment,IL-1 β,hs-CRP,TNF-α,PTX3 and Lp-PLA2 in both groups decreased significantly after 1 week and 2 weeks of treatment,the levels of IL-1 β,hs-CRP,TNF-α,PTX3 and Lp-PLA2 were lower in the observation group than those in the control group(P＜0.05).Conclusion Edaravone has significant therapeutic effects in AC1,which is beneficial for alleviating inflammatory reactions and improving neurological damage.Its protective mechanism may be related to the regulation of TLR4 NF-κ B pathway on factors associated with nerve injury and inflammatory responses.
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