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脑梗死患者认知功能障碍的TGFβ/Smad信号转导通路参与机制 被引量:9

Participation mechanism of TGFβ/ Smad signaling pathway in the pathogenesis of cognitive dysfunction in cerebral infarction patients
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摘要 目的探讨TGFβ/Smad信号转导通路在临床脑梗死病患认知功能障碍中的参与作用。方法 120例患者中首发脑梗死患者68例,再发脑梗死患者52例。脑梗死患者认知功能检查依据简易精神状况检测量表进行,TGFβ/Smad信号转导通路中组成分子TGFβ、Smad1、Smad3和Smad7的水平采用酶联免疫吸附测定法进行分析。以本院同期的健康体检者作为对照组。结果脑梗死患者的MMSE评分比对照组低(P<0.05),且再发脑梗死患者的评分比首发脑梗死患者的评分低(P<0.05);脑梗死认知功能障碍组患者的TGFβ、Smad1、Smad3和Smad7水平比对照组升高(P<0.05)。结论脑梗死患者患者存在明显的认知功能障碍,且其认知功能障碍的发生可能与患者血清中TGFβ、Smad1、Smad3和Smad7蛋白浓度的升高有关。 Objective To investigate the participation mechanism of TGFβ/Smad signaling pathway in the cognitive dysfunction in patients with cerebral infarction. Methods Among 120 patients with cerebral infarction, primary cerebral infarction was observed in 68 patients and recurrent cerebral infarction was observed in 52 patients. The cognitive function was evaluated by MMSE. The expressions of TGFβ, Smadl/3/7 were evaluated by ELISA. The normal people with health examination were designed as control group. Results The MMSE score in cerebral infarction patients was significantly lower than the control group (P 〈 0.05 ), and the MMSE score in the recurrent cerebral infarction patients was significantly lower than the primary cerebral infarction patients ( P 〈 0.05 ). Serum TGFβ and Smadl, Smad 3, Smad 7 in the cerebral infraction patients with cognitive dysfunction were significantly higher than those in the control group ( P 〈 0.05 ). Conclusion TGFβ, Smad1/3/ 7 are involved in the pathogenesis of patients with cerebral infarction, and the onset of cognitive dysfunction may be correlated with increasing of serum TGFβ,Smad1,Smad3 . Smad7 levels.
作者 李娟
出处 《实用临床医药杂志》 CAS 2015年第17期21-23,27,共4页 Journal of Clinical Medicine in Practice
关键词 脑梗死 TGFβ/Smad信号转导通路 认知功能障碍 再发脑梗死 cerebral infarction TGFβ/Smad signaling transduction pathway cognitive dysfunction recurrent cerebral infarction
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