[1]孙艳艳,师艳莉,程浩洋,等.β2-肾上腺素能受体通过β-抑制蛋白/细胞外调节蛋白激酶通路在病毒性心肌炎中的机制研究[J].陕西医学杂志,2025,54(1):52-56.[doi:DOI:10.3969/j.issn.1000-7377.2025.01.009]
　SUN Yanyan,SHI Yanli,CHENG Haoyang.Mechanism of β2-adrenergic receptor in viral myocarditis through β-arrestin/ERK1/2 pathway[J].,2025,54(1):52-56.[doi:DOI:10.3969/j.issn.1000-7377.2025.01.009]
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β2-肾上腺素能受体通过β-抑制蛋白/细胞外调节蛋白激酶通路在病毒性心肌炎中的机制研究
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《陕西医学杂志》[ISSN:1000-7377/CN:61-1281/TN]

卷:
54
期数:
2025年1期
页码:
52-56
栏目:
基础研究
出版日期:
2025-01-05

文章信息/Info

Title:
Mechanism of β2-adrenergic receptor in viral myocarditis through β-arrestin/ERK1/2 pathway
作者:
孙艳艳; 师艳莉; 程浩洋; 沈玉珏; 田洪森
(邯郸市中心医院心血管内科二病区,河北 邯郸 056000)
Author(s):
SUN Yanyan; SHI Yanli; CHENG Haoyang
(The second ward of the Department of Cardiovascular Medicine,Handan Central Hosipital,Handan 056000,China)
关键词:
病毒性心肌炎;  β2-肾上腺素能受体;  β-抑制蛋白/细胞外调节蛋白激酶通路;  心肌损伤;  心功能;  小鼠
Keywords:
Viral myocarditis;  Beta 2 adrenergic receptor;  β-arrestin/ERK1/2 pathway;  Myocardial injury;  Cardiac function;  Mice
分类号:
R 542.2
DOI:
DOI:10.3969/j.issn.1000-7377.2025.01.009
文献标志码:
A
摘要:
目的:探究β2-肾上腺素能受体(β2-AR)通过β-抑制蛋白(β-arrestin)/细胞外调节蛋白激酶(ERK1/2)通路在病毒性心肌炎(VMC)小鼠心肌损伤中的可能作用机制。方法: 将40只小鼠随机分为:对照组、VMC组、抑制β2-AR组及抑制β-arrestin组,每组10只。超声心动图检测小鼠Tie指数、射血分数(EF)及左室短轴缩短率(FS)。HE染色检测心肌组织病理结构; Tunel试剂盒检测心肌凋亡水平; 免疫荧光染色检测心肌组织β2-AR、β-arrestin、ERK1/2蛋白水平; ELISA试剂盒检测血清肌酸激酶(CK)、天冬氨酸氨基转移酶(AST)含量。结果: 与对照组比较,VMC组小鼠Tie指数增加,EF、FS减少(均P<0.05),小鼠心肌组织结构疏松紊乱、炎性细胞大量浸润,心肌细胞凋亡增加,心肌组织β2-AR、β-arrestin及ERK1/2表达增加,血清CK与AST含量增加(均P<0.05); 与VMC组比较,抑制β2-AR组小鼠Tie指数减少,EF、FS增加(均P<0.05),小鼠心肌组织损伤改善,心肌细胞凋亡减少,心肌组织β2-AR、β-arrestin及ERK1/2表达减少。与VMC组比较,抑制β-arrestin组小鼠心肌组织β-arrestin及ERK1/2表达减少,血清CK与AST含量减少(均P<0.05)。结论: 抑制β2-AR可通过下调β-arrestin/ERK1/2通路改善VMC小鼠心功能异常及心肌损伤。
Abstract:
Objective:To investigate the role of β2-adrenergic receptor(β2-AR)in myocardial injury in mice with viral myocarditis(VMC)through β-arrestin/extracellular regulated protein kinases(ERK1/2)pathway.Methods: Forty mice were randomly divided into control group,VMC group,β2-AR inhibition group and β-arrestin inhibition group,with 10 mice in each group.Tie index,ejection fraction(EF)and fractional shortening(FS)were measured by echocardiography.HE staining was used to detect the pathological structure of myocardial tissue.The level of myocardial apoptosis was detected by Tunel kit.The protein levels of β2-AR,β-arrestin and ERK1/2 in myocardial tissue were detected by immunofluorescence staining.Serum creatine kinase(CK)and aspartate aminotransferase(AST)levels were detected by ELISA kits.Results: Compared with the control group,the Tie index was increased,EF and FS were decreased in the VMC group(all P<0.05),the structure of myocardial tissue was loose and disordered,the infiltration of inflammatory cells was abundant,the apoptosis of myocardial cells was increased,and the expression of β2-AR,β-arrestin and ERK1/2 in myocardial tissue was increased.The serum levels of CK and AST were increased(all P<0.05).Compared with VMC group,the Tie index was significantly decreased,EF and FS were increased(all P<0.05),the myocardial injury was improved,the apoptosis of myocardial cells was decreased,and the expression of β2-AR,β-arrestin and ERK1/2 was decreased in myocardial tissue of mice in β2-AR inhibition group(all P<0.05).Compared with VMC group,the expression of β-arrestin and ERK1/2 in myocardial tissue and the contents of CK and AST in serum were decreased in β-arrestin inhibition group(all P<0.05).Conclusion:Inhibition of β2-AR can improve cardiac dysfunction and myocardial injury in VMC mice by down-regulating β-arrestin/ERK1/2 pathway.

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备注/Memo

备注/Memo:
基金项目:河北省医学科学研究课题(20220535)
更新日期/Last Update: 2025-01-06