RESUMO
【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 cross-sectional area (P<0.05) of μMT_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.