B淋巴细胞调控炎症细胞聚集促进血管紧张素Ⅱ/苯肾上腺素诱导的心肌肥厚  

B lymphocytes promote angiotensinⅡ/phenylephrine induced cardiac hypertrophy by regulating inflammatory cell aggregation

作　　者：王西强 刘成峰 刘平[2] 马爱群[2] 刘小祥[1] 石爽[1] WANG Xiqiang;LIU Chengfeng;LIU Ping;MA Aiqun;LIU Xiaoxiang;SHI Shuang(Department of Cardiovascular Medicine,Shaanxi Provincial People’s Hospital,Xi’an 710068;Department of Cardiovascular Medicine,The First Affiliated Hospital of Xi’an Jiaotong University,Xi’an 710061,China)

机构地区：[1]陕西省人民医院心血管内科,陕西西安710068 [2]西安交通大学第一附属医院心血管内科,陕西西安710061

出　　处：《西安交通大学学报（医学版）》2022年第5期671-677,共7页Journal of Xi’an Jiaotong University（Medical Sciences）

基　　金：陕西省人民医院科技人才支持计划(No.2021-JY-06);陕西省基础研究计划青年项目(No.2022JQ-855)。

摘　　要：目的探索B淋巴细胞在血管紧张素Ⅱ/苯肾上腺素(AngⅡ/PE)诱导的心室肥厚中的作用及其机制,以阐释炎症细胞在心肌损伤中的作用。方法使用AngⅡ/PE对野生型(WT)及B淋巴细胞缺乏型(μMT)小鼠作用2周或4周建立模型,并设立对照组。无创血压计评估小鼠血压,小鼠心动超声评估心脏结构及功能,流式细胞术及免疫荧光染色评估心脏炎症浸润,Masson染色评估心肌纤维化。结果AngⅡ/PE组小鼠左心室质量(P<0.01)、心脏质量/胫骨长度比(P<0.01)、心肌细胞横截面积与对照组相比明显增加(P<0.01)。AngⅡ/PE作用2周后,B淋巴细胞(P<0.05)、CD45^(+)白细胞(P<0.05)、CD64^(-)Ly6C^(+)单核细胞(P<0.05)、CD64^(+)Ly6C^(-)巨噬细胞(P<0.05)及Ly6g^(+)中性粒细胞(P<0.05)在心肌组织内大量聚集。与WT_AngⅡ/PE组相比,μMT_AngⅡ/PE小鼠心脏质量/胫骨长度比(P<0.05)、左心室质量(P<0.05)及心肌细胞横截面积(P<0.05)明显改善,心肌组织CD45^(+)Ly6C^(+)CD64^(-)单核细胞(P<0.05)和CD45^(+)Ly6C^(-)CD64^(+)巨噬细胞(P<0.05)明显减少。结论B淋巴细胞缺乏通过减少CD45^(+)Ly6C^(+)CD64^(-)单核细胞和CD45^(+)Ly6C^(-)CD64^(+)巨噬细胞的浸润,改善AngⅡ/PE所致的心室肥厚。Objective To explore B lymphocytes’role and mechanisms in angiotensinⅡ/phenylephrine(AngⅡ/PE)induced cardiomyopathy so as to understand the role of inflammatory cells in myocardial injury.Methods AngⅡ/PE was administered to wild-type(WT)and B cells deficiency(μMT)mice for 14 days or 28 days.The mice were analyzed by blood pressure measurement,echocardiography imaging,flow cytometry,and histology.Cardiac fibrosis was evaluated by Masson staining.Results Compared with the control group,the left ventricular mass(P<0.01),heart mass/tibia length ratio(P<0.01)and cross-sectional area of cardiomyocytes in AngⅡ/PE group were significantly increased(P<0.01).After 2 weeks of AngⅡ/PE treatment,B lymphocytes(P<0.05),CD45^(+)leukocytes(P<0.05),CD64^(-)Ly6C^(+)monocytes(P<0.05),CD64^(+)Ly6C^(+)macrophages(P<0.05)and Ly6g^(+)neutrophils(P<0.05)were recruited in myocardial tissue.Compared with WT_AngⅡ/PE group,the heart weight/tibia length ratio(P<0.05),left ventricular weight(P<0.05)and myocardial cell crosssectional area(P<0.05)ofμMT_AngⅡ/PE mice were significantly improved.CD45^(+)Ly6C^(+)CD64^(-)monocytes(P<0.05)and CD45^(+)Ly6C^(+)CD64^(+)macrophages(P<0.05)were significantly decreased.Conclusion B lymphocytes deficiency improves AngⅡ/PE induced cardiac hypertrophy by reducing the infiltration of CD45^(+)Ly6C^(+)CD64^(-)monocytes and CD45^(+)Ly6C^(+)CD64^(+)macrophages.

关 键 词：B淋巴细胞 血管紧张素Ⅱ/苯肾上腺素 心室肥厚 

分 类 号：R542.2[医药卫生—心血管疾病]