Boldina disminuye la apoptosis miocárdica post isquemia reperfusión en la rata

background: ischemia / reperfusion (ir) is relevant in the myocardial loss of cardiomyocytes through apoptosis. during ir, hemi channels (hc) allow the entry of proapoptotic substances to the cell. boldine, a compound extracted from peumus boldus, has proven to be antioxidant and to block hc. objective: to determine the effect of boldine on cardiomyocyte apoptosis in rats subjected to ir. methods: male rats, body weight (bw) 200 g, were subjected to reversible ligation of the left coronary artery for 30 minutes (i) and subsequent reperfusion (r) for 24 hours. a subset of these animals (ir+b) received an intraventricular dose of boldine (40mg/kg) and then two doses via gavage (75 mg/kg) at 30 and 60 minutes post-r. sham operated rats (s) receiving the same treatment were used as controls. we determined body weight (bw), relative heart mass (rhm) and systolic blood pressure (sbp). percentage of apoptotic cardiomyocytes (cmap), other apoptotic cells (ocap) and total apoptotic cells (tcap) were determined by tunel. activation of metalloproteinases (mmps) 2 and 9 was determined by zymography and mcp-1 mrna levels by rt-pcr. results: compared to ir alone, ir+boldine did not change bw or rcm, but significantly decreased pas, tcap (71 ± 2.4 vs 57 ± 1.5, p=0.016) and cmap (69 ± 1.5 vs 44 ± 0.4, p=0.016). no difference was observed in the ocap, mmps activity and mcp-1 mrna levels. conclusions: boldine decreased sbp and post-ir cardiomyocyte apoptosis without effect on other cells. this effect was not mediated by mmps activity or mcp-1 gene expression.