Abstract
BackgroundTaxifolin (TAX), is an active flavonoid, that plays an underlying protective role on the cardiovascular system. This study aimed to evaluate its effect and potential mechanisms on myocardial ischemia/reperfusion (I/R) injury.MethodsHealthy rat heart was subjected to I/R using the Langendorff apparatus. Hemodynamic parameters, including heart rate, left ventricular developed pressure (LVDP), maximum/minimum rate of the left ventricular pressure rise (+dp/dtmax and −dp/dtmin) and rate pressure product (RPP) were recorded during the perfusion. Histopathological examination of left ventricular was measured by hematoxylin-eosin (H&E) staining. Creatine kinase-MB (CK-MB) and lactate dehydrogenase (LDH) activities in the effluent perfusion, and the levels of malondialdehyde (MDA), superoxide dismutase (SOD), and glutathione peroxidase (GSH-PX) in the tissue were assayed. Apoptosis related proteins, such as B-cell lymphoma-2 (Bcl-2), Bcl2-associated X (Bax), and cytochrome c (Cyt-c) were also assayed by ELISA. Western blot was employed to determine apoptosis-executive proteins, including caspase 3 and 9. Transferase-mediated dUTP-X nick end labeling assay was performed to evaluate the effect TAX on myocardial apoptosis.ResultsTaxifolin significantly improved the ventricular functional recovery, as evident by the increase in LVDP, +dp/dtmax, −dp/dtmin and RPP, the levels of SOD, GSH-PX were also increased, but those of LDH, CK-MB, and MDA were decreased. Furthermore, TAX up-regulated the Bcl-2 protein level but down-regulated the levels of Bax, Cyt-c, caspase 3 and 9 protein, thereby inhibits the myocardial apoptosis.DiscussionTaxifolin treatment remarkably improved the cardiac function, regulated oxidative stress and attenuated apoptosis. Hence, TAX has a cardioprotective effect against I/R injury by modulating mitochondrial apoptosis pathway.
Highlights
Ischemic heart disease is a threat to human health
Effects of TAX on cardiac parameters of isolated hearts We examined whether TAX could protect the hearts of rat against ex vivo I/R injury
left ventricular developed pressure (LVDP) was significantly increased in the TAX 15 mM group compared with the I/R group at the end periods of reperfusion (LVDP = 68 vs. 52 mmHg, P < 0.05, Fig. 2B)
Summary
Ischemic heart disease is a threat to human health. Extracorporeal circulation and coronary bypass surgery are usually employed to improve myocardial ischemia after myocardial infarction occurs. This study aimed to evaluate its effect and potential mechanisms on myocardial ischemia/reperfusion (I/R) injury. Creatine kinase-MB (CK-MB) and lactate dehydrogenase (LDH) activities in the effluent perfusion, and the levels of malondialdehyde (MDA), superoxide dismutase (SOD), and glutathione peroxidase (GSH-PX) in the tissue were assayed. Apoptosis related proteins, such as B-cell lymphoma-2 (Bcl-2), Bcl2-associated X (Bax), and cytochrome c (Cyt-c) were assayed by ELISA. Results: Taxifolin significantly improved the ventricular functional recovery, as evident by the increase in LVDP, +dp/dtmax, -dp/dtmin and RPP, the levels of SOD, GSH-PX were increased, but those of LDH, CK-MB, and MDA were decreased. TAX has a cardioprotective effect against I/R injury by modulating mitochondrial apoptosis pathway
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