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Inhibition of TGF-β by a novel PPAR-γ agonist chrysin salvages β-receptor stimulated myocardial injury in rats through MAPKs-dependent mechanism

机译:新型PPAR-γ激动剂chrysin抑制TGF-β通过MAPKs依赖性机制挽救β受体刺激的大鼠心肌损伤

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摘要

BackgroundPharmacological stimulation of peroxisome proliferator-activated receptor-gamma (PPAR-γ) has been recognized as a molecular switch in alleviating myocardial injury through modulating oxidative, inflammatory and apoptotic signaling pathways. This study was designed to elucidate the effect of chrysin, a novel PPAR-γ agonist and its functional interaction with TGF-β/MAPKs in isoproterenol-challenged myocardial injury in rats.
机译:背景过氧化物酶体增殖物激活受体-γ(PPAR-γ)的药理刺激已被认为是通过调节氧化,炎症和凋亡信号通路减轻心肌损伤的分子开关。这项研究旨在阐明新的PPAR-γ激动剂chrysin的作用及其与TGF-β/ MAPKs在异丙肾上腺素激发的心肌损伤中的功能相互作用。

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