[1]李锦爽 王苗苗 徐子恒 高行娟 史册.NOX1在射血分数保留性心力衰竭中的表达特点及作用机制分析[J].心血管病学进展,2025,(6):579.[doi:10.16806/j.cnki.issn.1004-3934.2025.06.020]
　LI Jinshuang,WANG Miaomiao,XU Ziheng,et al.Mechanism Analysis of NOX1 Gene Expression on Heart Failure with Preserved Ejection Fraction[J].Advances in Cardiovascular Diseases,2025,(6):579.[doi:10.16806/j.cnki.issn.1004-3934.2025.06.020]
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NOX1在射血分数保留性心力衰竭中的表达特点及作用机制分析()

《心血管病学进展》[ISSN:51-1187/R/CN:1004-3934]

卷:
期数:
2025年6期
页码:
579
栏目:
论著
出版日期:
2025-06-25

文章信息/Info

Title:
Mechanism Analysis of NOX1 Gene Expression on Heart Failure with Preserved Ejection Fraction
作者:
李锦爽1 王苗苗2 徐子恒1 高行娟1 史册3
(1.徐州医科大学附属宿迁医院心血管内科,江苏 宿迁 223800;2. 徐州医科大学附属宿迁医院 护理部,江苏 宿迁 223800;3. 徐州医科大学附属宿迁医院 骨科,江苏 宿迁 223800)
Author(s):
LI Jinshuang1; WANG Miaomiao2; XU Ziheng1; GAO Xingjuan1; SHI Ce3
( 1.Department of Cardiology,The Affiliated Suqian Hospital of Xuzhou Medical University,Suqian 223800,Jiangsu,China;2.Nursing department,The Affiliated Suqian Hospital of Xuzhou Medical University,Suqian 223800, Jiangsu,China;3.Orthopedics,The Affiliated Suqian Hospital of Xuzhou Medical University,Suqian 223800,Jiangsu,China)
关键词:
射血分数保留性心力衰竭; NADPH氧化酶1; Alarin; 氧化应激
Keywords:
Heart failure with preserved ejection fraction; NOX1; Alarin; Oxidative stress
DOI:
10.16806/j.cnki.issn.1004-3934.2025.06.020
摘要:
目的 探讨Alarin/NOX1通路参与射血分数保留性心力衰竭（HFpEF）过程的分子机制，为HFpEF的治疗提供有效治疗靶点。方法 构建HFpEF动物模型，大鼠随机分为对照组、高盐饮食组、高盐饮食＋Alarin组、高盐饮食＋过表达对照组、高盐饮食＋NOX1过表达组以及高盐饮食＋Alarin＋NOX1过表达组。超声心动图检测大鼠E/e’、左心房面积的变化情况；ELISA法检测心肌组织中活性氧（ROS）、8-羟基脱氧鸟苷（8-OHdG）含量；HE染色检测心肌组织形态学变化；免疫组化检测心肌组织Alarin、NOX1的蛋白表达情况；Masson染色检测心肌组织胶原纤维沉积情况；蛋白质印迹法检测心肌组织中兰尼碱受体2（RyR2）、肌浆网钙泵（SERCA2）的表达情况。结果 高盐饮食＋Alarin组和高盐饮食＋Alarin＋NOX1过表达组左心房面积和E/e’指标显著下降；高盐饮食＋Alarin组和高盐饮食＋Alarin＋NOX1过表达组大鼠心肌组织中ROS、8-OHdG的含量显著降低；高盐饮食＋NOX1过表达组心肌细胞结构相对紊乱，心肌细胞横截面积增大，肌纤维增粗；Masson染色结果提示高盐饮食＋NOX1过表达组胶原纤维增多最明显；高盐饮食＋Alarin组大鼠心肌组织中RyR2蛋白表达水平显著降低，SERCA2蛋白表达水平显著升高。结论 NOX1在HFpEF患者中明显升高，Alarin 与 NOX1 结合改善氧化应激，调节降低的心肌舒张功能，从而改善 HFpEF 的心功能。
Abstract:
Objective Exploring the molecular mechanisms of NOX1/Alarin pathway involvement in the processes of HFpEF. Methods?/b>Dahl salt sensitive rats were used to create animal model s of HFpEF. The rats were randomly divided into a control group ,a high salt diet group,a high salt diet＋Alarin group,a high salt diet＋overexpression control group,a high salt diet＋NOX1 overexpression group,and a high salt diet＋Alarin＋NOX1 overexpression group,with 5 rats in each group. Changes in E/e’ and left atrial area of rats were detected by echocardiography;the ROS and 8-OHdG in myocardial tissue was detected by ELISA method; HE staining was used to detect morphological changes in myocardial tissue;Immunohistochemical detection of Alarin and NOX1 protein expression in myocardial tissue;Masson staining was used to detect the deposition of collagen fibers in myocardial tissue and evaluate myocardial fibrosis;the expression of RyR2 and SERCA2 in myocardial tissue was detected by Western blot. ResultsThe LA and E/e’ index significantly decreased in the high salt diet＋Alarin group and the high salt diet＋Alarin＋NOX1 overexpression group;the high salt diet＋Alarin group and the high salt diet＋Alarin＋NOX1 overexpression group significantly reduced the content of ROS and 8-OHdG in the myocardial tissue of rats;the high salt diet＋NOX1 overexpression group had relatively disordered myocardial cells structure,increased cross-sectional area of myocardial cells,and thickened muscle fibers;the high salt diet＋Alarin group significantly reduced the expression level of RyR2 protein in the myocardial tissue of rats,while the expression level of SERCA2 protein significantly increased. Conclusion NOX1 was significantly increased in HFpEF patients. NOX1 combined with Alarin to improve oxidative stress,thus improving the cardiac function of HFpEF.

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更新日期/Last Update: 2025-07-31