摘要
目的通过观察大鼠慢性压力负荷性心肌肥厚过程中左心室重塑2个时间点使用特异性COX-2抑制剂Celecoxib前后左心室质量指数(LVMI)、心脏重/体重比值和炎症标记物的变化,以了解中长期使用特异性COX-2抑制剂对左心室重塑的作用。方法将40只雄性SD大鼠随机分成5组:假手术组、手术20周组、Cele-coxib20周组、手术24周组、Celecoxib24周组。手术组及Celecoxib组均按照腹主动脉缩窄法制作压力负荷性心肌肥厚大鼠模型,在造模16周后,用Celecoxib10mg/kg,均匀混入饲料中喂服Celecoxib组大鼠,分别连续喂养4周和8周。在造模20周及24周时,观察大鼠左心室质量指数和炎症标记物TNF-α、TGF-β、PGE2、CRP、UA变化。结果手术组20和24周LVMI、TNF-α、PGE2、CRP、UA较假手术组均有升高(P<0.01,P<0.05);Celecoxib24周组LVMI及心脏重/体重比值、TNF-α、TGF-β、PGE2、CRP、UA均较手术组有下降(P<0.01,P<0.05)。结论炎症参与了心肌重塑的过程,特异性COX-2抑制剂Celecoxib可能通过抗细胞因子起到延缓左心室重塑发展。
Objective To investigate the changes in inflammation marker, LVMI and cardiac/body weight ratio in rats with left ventricle remodeling due to chronic pressure overload and the impact of long and medium - term usage COX -2 inhibitor Celecoxib on the remodeling of left ventricle remodeling. Methods Forty male Sprague - Dawley rats were randomly divided into 5 groups： Sham operated group, operated group 20 weeks, operated plus Celecoxib group 20 weeks, operated group 24 weeks, operated plus Celecoxib group 24 weeks. The operated group and operated plus Celecox- ib group underwent constriction of the abdominal aorta. At 16 weeks after operation, Celecoxib 10mg/kg was added to rat chow in the operated plus Celecoxib group. At 20 and 24 weeks after operation, serum levels of TNF - α, TGF - β, PGE2 and CRP were measured by ELISA. Uric acid was also measured. Results Compared to Sham operated group, the levels of TNF - β, PGE2, CRP and UA increased in operated group （ P 〈 0.05 ）. In comparison to the operated group, the levels of TNF - α, TGF - β, PGE2, CRP and UA decreased in operated add to Celecoxib group （P 〈 0.05）. Conclusion Inflammation participates in left ventricle remodeling. Selective cycloxygenase - 2 inhibitor Celecoxib may antagonize cytokines and slow down the development of left ventricle remodeling.
出处
《广东医学》
CAS
CSCD
北大核心
2009年第9期1235-1237,共3页
Guangdong Medical Journal
基金
广东省自然科学基金资助项目(编号:06022688)
关键词
左心室重塑
特异性COX-2抑制剂
炎症标记物
left ventricle remodeling
selective cycloxygenase- 2 inhibitor
inflammation marker
