H型高血压脑梗死患者TGFβ/Smad通路研究及黄芩苷的干预作用  

Analysis of TGFβ/ Smad signaling pathway in H hypertension patients with cerebral infarction and intervention function of baicalin

作　　者：赵博[1] 贺永进[1] 兰艳丽[1] 宋延斌[1] 

机构地区：[1]陕西省延安市延安大学附属医院东关心脑血管分院心内科一病区,陕西延安716000

出　　处：《实用临床医药杂志》2015年第17期15-17,共3页Journal of Clinical Medicine in Practice

摘　　要：目的探讨H型高血压脑梗死患者TGFβ/Smad通路参与作用及黄芩苷的改善作用。方法对120例H型高血压脑梗死患者进行分析,比较H型高血压脑梗死患者接受黄芩苷治疗前后血脂水平及TGFβ/Smad通路关键蛋白的表达。结果H型高血压脑梗死患者血清血脂水平及炎症因子水平明显高于对照组,TGFβ、Smad1和Smad3表达明显升高(P<0.05);黄芩苷治疗后上述异常得到显著改善(P<0.05)。结论 H型高血压脑梗死患者的发病可能与TGFβ/Smad通路的过度激活有关,而黄芩苷可以通过抑制TGFβ/Smad通路改善脑梗死患者血脂及炎症因子异常。Objective To analyze the involvement of Smad signaling pathway and improvement of baicalin in H hypertension patients with cerebral infarction. Methods A total of 120 H hypertension patients in our hospital were analyzed. The protein expression of TGFβ/Smad signaling pathway and blood lipid level before and after baicalin treatment were compared. Results The result revealed that the serum inflammatory factor concentration as well as TGFβ, Smadl and Smad3 expression were higher in H hypertension patients（P 〈 0.05）, and those abnormalities were alleviated greatly after the medication of Baicalin （P 〈 0.05）. Conclusion The activated Smad signaling pathway is involved in the pathogenesis of cerebral infarction and Baicalin alleviates abnormalities of blood lipid and inflammatory factors by inhibiting the Smad signaling pathway.

关 键 词：H型高血压 同型半胱氨酸 炎症因子 脑梗死 

分 类 号：R743.2[医药卫生—神经病学与精神病学]