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，因此具有廣譜的抗心律失常作用。苦參堿對冠脈結(jié)扎缺血、缺血再灌注、異丙腎上腺素、高血脂、糖尿病和阿霉素引起的心肌損傷都有保護(hù)作用。苦參堿還能阻滯心肌肥大和纖維化的發(fā)生、發(fā)展?？鄥A保護(hù)心臟作用的基本機(jī)制是抗氧化、抗炎、降血糖、調(diào)血脂作用，由此抑制ROS/TLR4信號通路、PI3K/Akt信號通路和TGF-β誘導(dǎo)的PERK信號通路，激活A(yù)kt和STAT3信號通路和AMPKα/UCP2信號通路，上調(diào)JAK2/STAT3通路上的HSP70以及JNK、ASK1、eNOS和一氧化氮的表達(dá)，提高線粒體ATP酶活性，保護(hù)線粒體而減少心肌細(xì)胞凋亡、減輕心肌損傷和抑制膠原合成，從而抑制心肌肥大和纖維化。從抗各種心肌缺血性損傷、抗阿霉素誘導(dǎo)的心肌損傷、抗高糖性心肌損傷、抗心肌肥大和纖維化4個方面綜述苦參堿的心臟保護(hù)作用及其機(jī)制。

Matrine has positive inotropic action, negative chronotropic action, and negative automatic action, so it possesses a broad-spectrum antiarrhythmic effect. Matrine has the protective action against myocardial injury induced by coronary artery ligature-induced ischemia, ischemia/reperfusion, isoproterenol, hyperlipoidemia, hyperglycemia, and adriamycin. Matrine can block to occurrence and development of myocardial hypertrophy and fibrosis. The basic mechanisms of cardioprotective effects of matrine are antioxidation, anti-inflammation, hypoglycemia, and hypolipemia, thus inhibiting signaling pathways of ROS/TLR4, PI3K/Akt, and TGF-β-induced PERK, and activating signaling pathways of Akt, STAT3, and AMPKα/UCP2, to up-regulate the expressions of HSP70 in JAK2/STAT3 pathway, JNK, ASR1, eNOS, and NO, and to increase activity of ATPase in mitochondria and to protect mitochondria, deceasing myocardial apoptosis, and preventing myocardial injury and collagen synthesis, so attenuating myocardial hypertrophy and fibrosis. This article reviews the cardioprotective effect and mechanism of matrine from four aspects:anti-myocardial ischemic injury, anti-adriamycin induced myocardial injury, anti-high glucose induced myocardial injury, and anti-myocardial hypertrophy and fibrosis.

R966