摘要
目的 检测在风湿性心脏病心房颤动（房颤）患者左心房中calpain-Ⅰ、calpastatin和caspase-3的含量以及细胞凋亡的发生率,探讨它们之间的相互关系,研究它们在房颤发病机制中的作用.方法 选择接受外科换瓣手术的风湿性心脏病患者共43例,分为三组;其中窦性心律组15例,阵发性房颤（阵发房颤）组8例,永久性房颤（永久房颤）组20例.在外科手术中取左心房组织,应用免疫印迹法测定各组患者的calpain-Ⅰ、calpastatin和caspase-3的蛋白含量;应用TUNEL法检测各组患者左心房肌细胞凋亡,计算其凋亡指数（AI）,分析比较它们之间的关系.结果 与窦性心律组比较：（1） 永久房颤组的calpain-Ⅰ含量增加到（344.0±101.9）%,caspase-3含量增加到（394.0±99.4）%（P＜0.01）,calpastatin含量降低到（27.0±12.8）%（P＜0.01）;而阵发房颤组的各蛋白含量则无明显变化;（2）永久房颤组左心房心肌细胞AI为（24.6±9.1）%,明显升高（P＜0.01）;（3）在永久房颤组中,calpain-Ⅰ和caspase-3的蛋白含量及AI分别与左心房内径、房颤持续时间呈明显正相关（P＜0.05～0.01）;calpastatin的蛋白含量却分别与两者呈明显负相关（P=0.007,P=0.001）;（4）calpain-Ⅰ的含量分别与caspase-3的含量、AI呈明显正相关（均为P＜0.01）;而calpastatin的含量分别与calpain-Ⅰ、caspase-3的含量明显负相关（均为P＜0.01）.结论 永久房颤时,左心房组织心肌细胞凋亡增加,calpain-Ⅰ、caspase-3、calpastatin蛋白表达出现变化,并且它们之间关系密切、相互影响,可能形成一个体系,使心房结构和功能改变,促使房颤发生和持续存在,可能是房颤发病的重要机制之一.
Objective The aim of the present study was to detect the expression of calpain-Ⅰ , calpastatin,caspase-3 and apoptosis in the left atria of patients with rheumatic heart disease （RHD）, and to find the association of these factors. Also, it was intended to investigate the effect of the above factors on the mechanism of atrial fibrillation （AF）. Methods 43 patients with RHD undergoing valve-replacement were included, 15 patients with regular sinus rhythm （ Group RSR）, 8 patients with paroxysmal AF （ Group AF1 ） and 20 patients with permanent AF （Group AF2）. Western blot was used to examine the content of calpain- Ⅰ, caspase-3 and calpastatin. The apoptosis index （ AI ） was measured by TUNEL. Results （ 1 ） Expression of calpain- Ⅰ in group AF2 was increased to （344.0 ± 101.9） %, and caspase-3 was increased to （394.0 ±99.4） % compared to group RSR （P 〈0.01, respectively）. Amount of calpastatin was reduced to （27.0 ± 12.8） % （P 〈 0.01 ）. The expressions of these proteins were unchanged in group AF1. （2） AI in group AF2 was higher than that in groups RSR and AF1 （P 〈0.01）. （3） In group AF2, the levels of calpain- Ⅰ , caspase-3 and AI were positively relative to left atrial dimension and AF duration, P 〈 0.05 - 0.01, respectively, whereas calpastatin was negatively correlated with left atrial dimension and AF duration （P =0.007 and P =0.001, respectively）. （4） The protein content of calpain- Ⅰ was positively related with that of caspase-3 and AI （ P 〈 0.01, respectively）, and the content of calpastatin was negatively related with that of calpain- Ⅰ and caspase-3 （P 〈 0.01, respectively）. Conclusions Apoptosis of atrial cell increased in left atria and the protein contents of calpain- Ⅰ, caspase-3 and calpastatin significantly altered during AF in humans with RHD. The observed interactions suggest that these factors compose a system to cause the structural remodeling and dysfunction of atria. The course may play a key role in promoting the onset and maintenance of AF.
出处
《中华心血管病杂志》
CAS
CSCD
北大核心
2006年第4期303-307,共5页
Chinese Journal of Cardiology
