氧化苦參堿對心臟具有正性肌力、負(fù)性頻率和負(fù)性自律性的作用，因此具有廣譜抗心律失常作用。氧化苦參堿對冠脈狹窄缺血、缺血再灌注以及異丙腎上腺素、阿霉素、感染和免疫引起的心肌損傷都有保護(hù)作用，并能阻滯心肌肥大和纖維化發(fā)生發(fā)展。氧化苦參堿心臟保護(hù)作用的基本機(jī)制是其抗氧化、抗炎和免疫抑制以及抑制鹽皮質(zhì)激素（醛固酮）受體的表達(dá)，產(chǎn)生心肌保護(hù)作用。即通過激活Nrf2/HO-1信號通路和抑制轉(zhuǎn)化生長因子（TGF）-β1及I型TGF-β1受體的表達(dá)，從而抑制下游的JAK/STAT、MAPK/Smad2/3和Notch的信號通路的機(jī)制，減少心肌細(xì)胞凋亡，減輕心肌損傷和抑制膠原合成，產(chǎn)生抑制心肌肥大和纖維化的作用。

Oxymatrine has positive inotropic action, negative chronotropic action, and negative automatic action, so it possesses a braod-spectrum antiarrhythmic effect. Oxymatrine has the protective actions against myocardial injuries induced by coronary artery stricture-induced ischemia, ischemia/reperfusion, isoproterenol, adriamycin, infection and immunization, Oxymatrine can block to occurrence and development of myocardial hypertrophy and fibrosis. The basic mechanisms of cardioprotective effect of oxymatrine are antioxidation, anti-inflammation, immunodepression, and down-regulating the expression of mineralocorticoid (aldosterone) receptor, thus activating Nrf2/HO-1 pathway, and inhibiting the expression of TGF-β1 and its I type receptor, therefore blocking backward signaling pathways of JNK/STAT, MAPK/Smad2/3, and Notch, to decrease myocardial apoptosis, and prevent myocardial injury and collagen synthesis, so to express the attenuating effects of myocardial hypertrophy and fibrosis.

R285.5