Abstract: OBJECTIVE To study the effect and mechanism of notoginsenoside R1 on myocardial injury in rats with coronary heart disease. METHODS Rats were randomly divided into control group, model group, notoginsenoside R1 low, medium and high dose group, 9 rats in each group. Rat model of coronary heart disease was established by intraperitoneal injection of high fat diet combined with posterior pituitary injection. The notoginsenoside R1 low, medium and high dose group were administered with notoginsenoside R1 50, 100 and 200 mg·kg^-1 by gavage once a day for 4 weeks. Myocardial injury was observed by HE staining. The expression of cleaved caspase-3 and caspase-9 was detected by Western blotting. Mean ventricular systolic pressure, heart rate and left ventricular systolic pressure levels were measured. Heart damage markers myoglobin(Mb), creatine kinase isozyme(CK-MB) and cardiac troponin(cTnI) expression levels and inflammatory factors interleukin-6(IL-6), interleukin-1β(IL-1β), inducible nitric oxide synthase(iNOS) and tumor necrosis factor-α(TNF-α) contents were detected by ELISA. Myocardial cell malondialdehyde(MDA), superoxide dismutase(SOD), lactate dehydrogenase(LDH) and glutathione (GSH) expression levels were detected by the kit. Phosphorylation of adenosine monophosphate-activeted protein kinase(AMPK) and transcription factor NF-E2 related factor(Nrf2), heme oxygenase-1(HO-1) expression level was detected by Western blotting. RESULTS Notoginsenoside R1 reduced the degree of myocardial injury in rats with coronary heart disease, inhibited the expression of myocardial apoptosis proteins caspase-3 and caspase-9(P<0.05), up-regulated the levels of cardiac function indicators mean ventricular systolic pressure, heart rate and left ventricular systolic pressure(P<0.05), inhibited the high expression of heart injury markers CK-MB, cTnI and Mb(P<0.05), reduced the levels of oxidative stress indicators SOD, GSH, LDH and MDA(P<0.05), inhibited the expression of inflammatory factors IL-6, IL-1β, iNOS and TNF-α(P<0.05) and up-regulated the expression of AMPK/Nrf-2/HO-1 signal pathway(P<0.05). CONCLUSION Notoginsenoside R1 improves myocardial injury in rats with coronary heart disease, inhibits cardiomyocyte apoptosis, oxidative stress, and inflammatory response, which is related to the activation of AMPK/Nrf-2/HO-1 signaling pathway.