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Low‐intensity pulsed ultrasound ameliorates angiotensin II-induced cardiac fibrosis by alleviating inflammation via a caveolin-1-dependent pathway 被引量:3

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摘要 Objective:Cardiac hypertrophy and fibrosis are major pathological manifestations observed in left ventricular remodeling induced by angiotensin II(AngII).Low-intensity pulsed ultrasound(LIPUS)has been reported to ameliorate cardiac dysfunction and myocardial fibrosis in myocardial infarction(MI)through mechano-transduction and its downstream pathways.In this study,we aimed to investigate whether LIPUS could exert a protective effect by ameliorating AngII-induced cardiac hypertrophy and fibrosis and if so,to further elucidate the underlying molecular mechanisms.Methods:We used AngII to mimic animal and cell culture models of cardiac hypertrophy and fibrosis.LIPUS irradiation was applied in vivo for 20 min every 2 d from one week before mini-pump implantation to four weeks after mini-pump implantation,and in vitro for 20 min on each of two occasions 6 h apart.Cardiac hypertrophy and fibrosis levels were then evaluated by echocardiographic,histopathological,and molecular biological methods.Results:Our results showed that LIPUS could ameliorate left ventricular remodeling in vivo and cardiac fibrosis in vitro by reducing AngII-induced release of inflammatory cytokines,but the protective effects on cardiac hypertrophy were limited in vitro.Given that LIPUS increased the expression of caveolin-1 in response to mechanical stimulation,we inhibited caveolin-1 activity with pyrazolopyrimidine 2(pp2)in vivo and in vitro.LIPUS-induced downregulation of inflammation was reversed and the anti-fibrotic effects of LIPUS were absent.Conclusions:These results indicated that LIPUS could ameliorate AngII-induced cardiac fibrosis by alleviating inflammation via a caveolin-1-dependent pathway,providing new insights for the development of novel therapeutic apparatus in clinical practice.
出处 《Journal of Zhejiang University-Science B(Biomedicine & Biotechnology)》 SCIE CAS CSCD 2021年第10期818-838,共21页 浙江大学学报(英文版)B辑(生物医学与生物技术)
基金 This work was supported by the National Natural Science Foundation of China(No.81627802) the Priority Academic Program Development of Jiangsu Higher Education Institutions(No.PAPD2014-2016) the National Key R&D Program of China(No.2019YFA0210100).
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