Why the study?
Taxifolin is an active flavonoid with an underlying protective role in the cardiovascular system, but its effect and mechanisms in myocardial ischemia/reperfusion injury needed evaluation.
Does Taxifolin protect against myocardial ischemia/reperfusion injury in a rat model?
Does Taxifolin protect against myocardial ischemia/reperfusion injury in a rat model?
Taxifolin exerts cardioprotective effects against ischemia/reperfusion injury in a rat model by reducing oxidative stress and modulating the mitochondrial apoptosis pathway.
Answers are grounded in this paper and cite their sources.
Supports taxifolin investigation in rat ischemia/reperfusion models; leaves open clinical translation pending human trials.
Background Taxifolin (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. Methods Healthy 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 (+d p /d t max and −d p /d t min ) 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. Results Taxifolin significantly improved the ventricular functional recovery, as evident by the increase in LVDP, +d p /d t max , −d p /d t min 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. Discussion Taxifolin 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.
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Tang et al. (2019) studied this question.
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