新疆医科大学学报

目的 观察脑梗死后认知功能障碍患者采用重酒石酸卡巴拉汀胶囊联合胞二磷胆碱的治疗效果。方法 将2023年1月至2024年1月上海健康医学院附属崇明医院92例脑梗死后认知功能障碍患者按随机数字表法分为对照组和观察组，各46例。对照组采用胞二磷胆碱治疗，观察组于对照组基础上联合重酒石酸卡巴拉汀胶囊治疗。两组均连续治疗8周。比较两组治疗后认知功能、日常生活能力、血清神经细胞因子水平、沉默信息调节因子-1(SIRT1)/核因子-κB(NF-κB)信号通路相关指标及不良反应发生情况。结果 治疗后，观察组蒙特利尔认知评估量表(MoCA)评分、简易精神状况检查量表(MMSE)评分、Barthel指数评定量表(BI)评分、SIRT1、神经生长因子(NGF)和脑源性神经营养因子(BDNF)水平均高于对照组(P<0.05),S100蛋白、神经元特异性烯醇化酶(NSE)、NF-κB均低于对照组(P<0.05);观察组不良反应发生率同对照组比较差异无统计学意义(P>0.05)。结论 重酒石酸卡巴拉汀胶囊联合胞二磷胆碱能显著减轻脑梗死后认知功能障碍，其机制可能与调节SIRT1/NF-κB信号通路有关。

Objective To observe the therapeutic effect of carbalatine bitartrate capsule combined with citicoline in patients with cognitive dysfunction after cerebral infarction. Methods From January 2023 to January 2024, 92 patients with cognitive dysfunction after cerebral infarction in the hospital were divided into a control group and an observation group using the random number table method, with 46 patients in each group. The control group was treated with citicoline, while the observation group received additional rivastigmine tartrate capsules on the basis of the control group′s treatment. Both groups were treated continuously for 8 weeks. The cognitive function, daily living ability, serum neurocytokine level, silence-information regulator-1(SIRT1)/nuclear factor-κB(NF-κB) signaling pathway and the incidence of adverse reactions were compared between the 2 groups after thetreatment. Results After 8 weeks of the treatment, the Montreal Cognitive Assessment(MoCA) score, Mini-Mental State Examination(MMSE), Barthel Index(BI) score, SIRT1, nerve growth factor(NGF) and brain-derived neurotrophic factor(BDNF) levels the observation group were higher than those in the control group(P<0.05), while S100 protein, neuron-specific enolase(P>0.05), and NF-κB were lower than those in control group(P<0.05); there was no significant difference in the incidence of adverse between the observation group and the control group(P>0.05). Conclusion The combination of rivastigmine tartrate capsules and cytidine diphosphate choline can significantly alleviate cognitive impairment after cerebral infction, which may be related to the regulation of the SIRT1/NF-κB signaling pathway.