Effect of Xuenaoxin capsule on expression of endothelin and calcitonin gene-related peptide in patients with acute cerebral infarction
- VernacularTitle:血脑欣胶囊对急性缺血性中风患者血浆内皮素及降钙素基因相关肽的干预作用
- Author:
Baoling LI
;
Furun ZHAO
;
Lijun LIU
;
Xiaoxia ZHAO
;
Tianlin HOU
;
Jing LI
- Publication Type:Journal Article
- Keywords:
Acute cerebral infarction;
Xuenaoxin capsule;
Endothelin;
Calcitonin gene-related peptide;
Qi stagnation and blood stasis syndrome;
Clinical research
- From:
China Journal of Traditional Chinese Medicine and Pharmacy
2005;0(11):-
- CountryChina
- Language:Chinese
-
Abstract:
Objective:To observe the influences of Xuenaoxin capsule on the levels of endothelin(ET)and calcitonin gene-related peptide(CGRP)and neurological deficit extent in patients with acute cerebral infarction.Methods:A randomized, positive drug controlled clinical trial design was used,59 cases of acute cerebral infarction with qi stagnation and blood stasis syndrome were randomly divided into treatment group(30cases)and control group(29cases).The treatment group was treated with Xuenaoxin capsule,3 times a day,4 pills each time and the control group was treated with Nimodiping,3 times a day,20mg each time.Both groups had 14 days as a treatment course.The changes of levels of endothelin(ET)and calcitonin gene-related peptide(CGRP)in plasma as well as neurological deficit were measured and compared.Results:The plasma ET in treatment group (57.658?14.877)pg/L were significantly lower than those in control group(70.456?17.059)pg/L,but the plasma CGRP(84.404? 8.705)ng/L was higher than that in the control group(78.402?10.699)ng/L on the 14th day.The differences were both significant (P=0.0032,P=0.0213).The results showed that the total effective rate of Xuenaoxin capsule on improving clinical symptoms of patients with acute ischemic stroke was 76.67%and very superior to that of Nimodiping(P=0.0035).Conclusion:Xuenaoxin capsule could reduce neurological deficit extent,and improve the prognosis of patients with acute cerebral infarction by means of regulating ET and CGRP.