右美托咪定诱导心肌细胞代偿性肥大发挥心肌保护作用实验研究  

Dexmedetomidine induces compensatory hypertrophy of cardiomyocytes and plays a myocardial protective role

作　　者：曹雪峰[1] 赵亮[2] 刘旭东[3] 段凤梅[1] 董天鑫[1] 姬云飞[3] CAO Xuefeng;ZHAO Liang;LIU Xudong;DUAN Fengmei;DONG Tianxin;JI Yunfei(Department of Anesthesiology,Affiliated Hospital of Chengde Medical College,Chengde 067000,China;不详)

机构地区：[1]承德医学院附属医院麻醉科,河北承德067000 [2]承德医学院药理教研室,河北承德067000 [3]承德市中心医院麻醉疼痛科,河北承德067000

出　　处：《陕西医学杂志》2023年第7期783-787,共5页Shaanxi Medical Journal

基　　金：国家自然科学基金资助项目(81700310);河北省重点研发计划项目(22377746D);河北省承德市科学技术研究与发展计划项目(201904A099)。

摘　　要：目的:探讨右美托咪定(DEX)诱导心肌细胞代偿性肥大从而发挥心肌保护作用。方法:新生乳鼠(1~3 d)心脏提取分离培养,建立离体心肌细胞群。实验分组:正常心肌细胞对照组(C组)、DEX组(D组)。荧光显微镜观察两组心肌细胞的形态变化,Western blot检测两组心肌细胞肥大指标的差异表达,CCK8检测细胞活性。血管紧张素Ⅱ(AngⅡ)诱导心肌细胞肥大,建立离体心肌肥厚模型(A组),药物孵育24 h后停药24 h,Western blot检测三组细胞心房利钠肽(ANP)、脑利钠肽(BNP)和β-肌球蛋白重链基因(β-MHC)蛋白的表达水平。结果:与C组对比,D组心肌细胞形态增大;心肌肥大相关指标ANP、BNP和β-MHC蛋白水平表达增加,差异有统计学意义(均P<0.05);CCK8检测细胞活性增高,差异有统计学意义(P<0.05);D组停药后ANP、BNP和β-MHC蛋白表达明显恢复,接近C组。而A组停药后ANP、BNP和β-MHC蛋白表达并未恢复正常。结论:右美托咪定可能是通过诱导大鼠心肌细胞可逆代偿性肥大来保护心肌细胞的功能。Objective:To investigate the protective effect of dexmedetomidine(DEX)on cardiomyocytes by inducing compensatory hypertrophy.Methods:Neonatal rat hearts(1 to 3 days)were extracted,isolated and cultured to establish isolated cardiomyocyte populations.The experimental groups were normal cardiomyocytes control group(group C)and DEX group(group D).The morphological changes of cardiomyocytes in the two groups were observed by fluorescence microscope.The differential expression of cardiomyocyte hypertrophy indexes were detected by Western blot.The cell activity was detected by CCK8.AngiotensinⅡwas used to induce cardiomyocyte hypertrophy in vitro(group A).After 24 hours of incubation,the protein expression levels of atrial natriuretic peptide(ANP),brain natriuretic peptide(BNP)andβ-myosin complex(β-MHC)in the three groups were detected by Western blot.Results:Compared with group C,the morphology of cardiomyocytes in the group D was enlarged;the protein levels of ANP,BNP andβ-MHC increased(all P<0.05);the cell viability was increased(P<0.05).The protein expressions of ANP,BNP andβ-MHC in group D recovered significantly after drug withdrawal,which was close to that in group C.However,the expressions of ANP,BNP andβ-MHC did not return to normal after drug withdrawal in group A.Conclusion:Dexmedetomidine may protect the function of rat cardiomyocytes by inducing reversible compensatory hypertrophy.

关 键 词：右美托咪定 心肌肥大 心脏保护 乳鼠 血管紧张素Ⅱ 代偿 

分 类 号：R361.3[医药卫生—病理学]