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- W2368509384 abstract "Objective To explore the impact of isoproterenol(ISO) on myocardial apoptosis in mice.Methods Briefly,30 adult male mice were randomly divided into 3 groups and received continuously treatment with vehicle,ISO[30 mg/(kg·d)] or ISO+p38 inhibitor SB203580[10 mg/(kg·d)]through mini-osmotic pump implanted subcutaneously for 7 days,and heart tissue and plasma were collected for further assay.Results Consistent with the previous research,chronic ISO stimulation induced markedly apoptosis.Further study indicated that ISO could induce iNOS expression(63%),increase cytokine production(IL-6 and TNF-α),plasma NO and heart nitrotyrosine production.SB203580 administration blocked the p38 activity thus reduced cytokine production.It also inhibited iNOS expression,decreased plasma NO and heart nitrotyrosine content[ISO+SB203580 group vs ISO group,NO:(38.60± 6.60) μmol/g protein vs(58.80± 13.28)μmol/g protein,Nitrotyrosine:(2.86±0.43)μg/g protein vs(4.20±0.47) μg/g protein,P0.01],reduced plasma and heart IL-6 and TNF-α levels[ISO+SB203580 group vs ISO group,IL-6:(22.26±6.38) ng/L vs(51.32±9.20) ng/L,TNF-α:(11.75±1.09) ng/L vs(8.64±1.01)ng/L,P0.01].Moreover,it reduced heart hypertrophy and apoptosis.Conclusion Chronic ISO stimulation can induce cardiomyocyte apoptosis.With the previous results that iNOS inhibitor 1400w also reduced cardiac hypertrophy and apoptosis while have no effect on plasma CRP increasing,ISO may exert its proapoptotic effects by p38-cytokine-iNOS-ONOO-pathway." @default.
- W2368509384 created "2016-06-24" @default.
- W2368509384 creator A5068407474 @default.
- W2368509384 date "2010-01-01" @default.
- W2368509384 modified "2023-09-24" @default.
- W2368509384 title "Chronic isoproterenol stimulation induces cardiomyocyte apoptosis through p38-cytokine-iNOS pathway" @default.
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