Sympathetic nerve overactivity is one of the important pathological characters in chronic heart failure(CHF),and is the key factor accelerating the deterioration of CHF.The aim of this study was to e-lucidate the intrinsic mechanism of long chain non-coding RNA(lncRNA)heart failure-related regulator in paraventricular nuclei(PVN)regulate type 2 small conductance calcium-activated potassium channel(SK2)protein involved in the occurrence and development of CHF.The CHF rat model was established by ligation of the left anterior descending branch of the coronary artery.Down-regulated lncRNA HFAR was screened from the hypothalamic PVN tissue of CHF rats and the hypothalamic neurons incubated with an-giotensin Ⅱ(ANGⅡ)by qRT-PCR method(p＜0.001).Furthermore,investigation with cardiac ultra-sound detection,sympathetic nerve discharge recording methods,immunofluorescence and western blot technology indicated that overexpression of lncRNA HFAR in PVN can significantly improve the cardiac function,inhibit sympathetic nerve overactivity and upregulate SK2 expression in rats with CHF(p＜0.05).The results show that down-regulated lncRNA HFAR in PVN was involved in the regulation of sympathetic nerve overactivity in CHF rats by targeting SK2,which provides a new strategy for the treat-ment of CHF.
维普
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