RESUMEN
Objective To explore the effects of fistular onion bulb extract (FOB) on myocardial ischemia / reperfusion (I / R) injury and possible regulation mechanism. Methods The left anterior descending (LAD) artery of 36 adult rat heart was ligated for 30 minutes and subsequently released for 120 minutes to establish the I / R injury model in vivo. Cultured neonatal rat cardiomyocytes were subjected to 6 hours of hypoxia followed by 18 hours of reoxygenation to establish the hypoxia / reoxygenation (H / R) model in vitro. The rats or cardiomyocytes were randomly divided into the control group, I / R group (or H / R group) and FOB pretreatment+I / R group (or H / R group). The left ventricular (LV) function was measured using PowerLab multichannel physiological recorder; the infarct size was detected by 2, 3, 5-triphenyl tetrazolium chlorid(TTC) staining. The apoptosis rate was detected by flow cytometry, Western blotting and Real-time PCR were used to detect the expression of apoptosis-related proteins and mRNA (Bcl-2, Bax and Caspase-3); Immunofluorescence was used to detect the expression of cytochrome C (Cyt-C). Results In the animal experiments, compared with the control group, the left ventricular systolic and diastolic functions were deteriorated (P<0. 05); compared with the I / R group, the pretreatment of FOB significantly improved the left ventricular systolic and diastolic function, and decreased the infarct size (P<0. 05). In cultured cardiomyocytes, compared with the control group, the apoptosis rate was significantly increased (P<0. 01), the protein and mRNA expression of Bcl-2 decreased, meanwhile the expression of Bax, Caspase-3 and Cyt-C increased in the H / R group (P< 0. 05); Compared with the H / R group, the pretreatment of FOB significantly reduced the apoptosis rate (P < 0. 05), increased the protein and mRNA expression of Bcl-2, at the same time, decreased the expression of Bax, Caspase-3 and Cyt-C(P<0. 05). Conclusion Fistular onion bulb extract has the protective effect on myocardial ischemia / reperfusion injury, and its possible mechanism is to reduce cardiomyocyte apoptosis through mitochondrial pathway.