背景：丹参，丹参（唇形科）和红花的干燥根和根茎，红花（菊科）的干花作为草药对用于治疗心血管疾病（CVD）。
目的：研究DHHP对MIRI的影响及其基于细胞凋亡和线粒体的机制。
方法:36只SD大鼠(n=6)随机分为对照组,缺血再灌注组(IR)，阳性对照(新宁片，XNT,1g/kg/d）和DHHP（1.2、2.4和4.8g/kg/d）。除了Con,其他组胃内给药5d，分离大鼠心脏，建立MIRI体外模型，评价DHHP对MIRI的影响。24只SD大鼠(n=6)随机分为Con,IR,DPPH2.4（2.4g/kg/d）和DPPH2.4+白术苷（ATR）（2.4+5mg/kg/d），胃内给药5d，DPPH2.4+ATR组腹腔注射ATR(5mg/kg/d),取大鼠心脏建立MIRI体外模型以揭示其作用机制。
结果：心肌梗死面积为，分别,0.35%,40.09%,15.84%，30.13%,NAD+的浓度(nmol/gw/w)分别为144、83、119和88，在Con,IR,DHHP2.4、DHHP2.4+ATR组。裂解的caspase-3分别为0.3、1.6、0.5和1.3%，裂解的caspase-9分别为0.2、1.1、0.4和0.8%，分别,在Con,IR,DHHP2.4和DHHP2.4+ATR组。DHHP对MIRI的有益作用被ATR逆转。
结论：DHHP对MIRI的改善可能与抑制MPTP开放有关，减少氧化损伤，减轻缺血损伤，抑制心肌细胞凋亡。
BACKGROUND: Danshen, the dried root and rhizome of Salvia miltiorrhiza Bunge (Labiatae) and honghua, the dried flower of Carthamus tinctorius L. (Compositae) as the herb pair was used to treat cardiovascular diseases (CVD).
OBJECTIVE: To
study the effects of DHHP on MIRI and mechanisms based on apoptosis and mitochondria.
METHODS: 36 SD rats (n = 6) were randomly divided into control group (Con), the ischaemia-reperfusion group (IR), positive control (Xinning tablets, XNT, 1 g/kg/d) and DHHP (1.2, 2.4, and 4.8 g/kg/d). Except for Con, the other groups were intragastrically administrated for 5 d, the rat hearts were isolated to establish the MIRI model in vitro for evaluating the effects of DHHP on MIRI. 24 SD rats (n = 6) were randomly divided into Con, IR, DPPH2.4 (2.4 g/kg/d) and DPPH 2.4 + Atractyloside (ATR) (2.4 + 5 mg/kg/d), administered intragastrically for 5 d, then treated with ATR (5 mg/kg/d) by intraperitoneal injection in DPPH2.4 + ATR group, took rat hearts to establish MIRI model in vitro for revealing mechanism.
RESULTS: Myocardial infarct sizes were, respectively, 0.35%, 40.09%, 15.84%, 30.13%, concentrations of NAD+ (nmol/gw/w) were 144, 83, 119, and 88, respectively, in Con, IR, DHHP2.4, DHHP2.4 + ATR group. Cleaved caspase-3 were 0.3, 1.6, 0.5 and 1.3% and cleaved caspase-9 were 0.2, 1.1, 0.4 and 0.8%, respectively, in Con, IR, DHHP2.4 and DHHP2.4 + ATR group. The beneficial effects of DHHP on MIRI were reversed by ATR.
CONCLUSIONS: The improvement of MIRI by DHHP may be involved in inhibiting MPTP opening, decreasing oxidative damage, alleviating ischaemic injury and inhibiting cardiomyocyte apoptosis.
