目的:观察脑复聪方联合尼莫地平治疗脑小血管病合并认知功能障碍的临床疗效。方法:122例脑小血管病合并认知功能障碍患者按照随机数字表法随机分为对照组62例和观察组60例。对照组给予基础治疗及尼莫地平,观察组在对照组治疗基础上给予脑复聪方治疗,共治疗3个月。治疗后,比较两组患者临床疗效及安全性,治疗前后中医证候积分、蒙特利尔认知评估量表(Montreal cognitive assessment Scale,MoCA)评分、简易精神状态量表(mental state scale,MMSE)评分、日常生活能力量表(ability of daily living scale,ADL)评分,比较两组治疗前后血清S100β、白细胞介素-8(interleukin-8,IL-8)水平。结果:治疗后,观察组有效率(95.00%)显著高于对照组(80.65%)(P<0.05);两组患者中医证候积分均高于本组治疗前(P<0.05),且观察组中医证候积分均高于同期对照组(P<0.05);两组患者MoCA评分各维度得分及总分均高于本组治疗前,且观察组高于同期对照组(P<0.05);两组患者MMSE评分各维度得分及总分、ADL评分均显著高于治疗前,且观察组高于同期对照组(P<0.05);两组患者血清S100β、IL-8水平显著低于本组治疗前,且观察组低于同期对照组(P<0.05)。治疗期间两组患者血尿常规、心电图及肝肾功能检查均未出现明显异常。结论:脑复聪方联合尼莫地平治疗脑小血管病合并认知功能障碍疗效显著,能显著改善患者认知功能及自理能力,减轻脑损伤程度,且安全性较高。
Objective: To determine the effect of medicated serum of Chinese herbal compound Naofucong(脑复聪, NFC) on the microglia BV-2 cells viability and the transcription and expression of interleukin-6(IL-6) and tumor necrosis factor α(TNF-α) in microglia BV-2 cells to further explore the mechanisms underlying the protective effect of NFC on inflammatory process induced by high glucose. Methods: The microglia BV-2 cells incubated in vitrowere divided into different groups: the control group(25 mmol/L glucose), the model group(75 mmol/L glucose), high glucose media containing different dose medicated serum of NFC. After being cultured for 24 h, changes in IL-6 and TNF-α were measured by quantitative real-time polymerase chain reaction and enzyme-linked immunosorbent assay. The expression of surface marker CD11 b of activated microglia was measured by confocal laser scanning microscope and Western blot. Nuclear factor-κB(NF-κB) p-p65 expression was analyzed by Western blot. Results: The model group obviously increased the expression of microglial surface marker CD11 b and NF-κB p-p65(all P<0.01), induced a significant up-regulation of release and the m RNA expression of IL-6 and TNF-α(P<0.01 or P<0.05). The medicated serum of NFC could obviously down-regulate the transcription and expression of surface marker CD11 b and NF-κB p-p65(all P<0.01), and inhibit the m RNA and protein expression(P<0.01 or P<0.05) of inflammatory cytokines, such as IL-6 and TNF-α, in microglia BV-2 cells cultured with high glucose for 24 h. Conclusions: The inhibition of microglial activation and IL-6 and TNF-α expression induced by high glucose may at least partly explain NFC therapeutic effects on diabetes-associated cognitive decline diseases. Its underlying mechanism could probably be related to the inhibition of NFC on NF-κB phosphorylation.
