Taxifolin protects rat against myocardial ischemia/reperfusion injury by modulating the mitochondrial apoptosis pathway

doi:10.7717/peerj.6383

Paper

Taxifolin protects rat against myocardial ischemia/reperfusion injury by modulating the mitochondrial apoptosis pathway

Published Jan 31, 2019 · Zhenqiu Tang, Chunjuan Yang, Baoyan Zuo

PeerJ

Q1 SJR score

29

Citations

0

Influential Citations

Full textSemantic Scholar

Abstract

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 (+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. 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 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.

Non-RCT

Animal Study

Rigorous Journal

Study Snapshot

Taxifolin improves cardiac function, regulates oxidative stress, and inhibits myocardial apoptosis by modulating the mitochondrial apoptosis pathway.

PopulationOlder adults (50-71 years)

Sample size24

MethodsObservational

OutcomesBody Mass Index projections

ResultsSocial networks mitigate obesity in older groups.

Sign up to use Study Snapshot

Consensus is limited without an account. Create an account or sign in to get more searches and use the Study Snapshot.

Create an account

Paper

Taxifolin protects rat against myocardial ischemia/reperfusion injury by modulating the mitochondrial apoptosis pathway

Sign up to use Study Snapshot

References

Early Prediction of Hypoxic-Ischemic Brain Injury by a New Panel of Biomarkers in a Population of Term Newborns

A new panel of oxidative stress biomarkers can effectively predict early hypoxic-ischemic brain injury in term newborns, with higher levels associated with higher brain damage severity.

Fisetin Confers Cardioprotection against Myocardial Ischemia Reperfusion Injury by Suppressing Mitochondrial Oxidative Stress and Mitochondrial Dysfunction and Inhibiting Glycogen Synthase Kinase 3β Activity

Fisetin effectively reduces myocardial ischemia/reperfusion injury by suppressing mitochondrial oxidative stress and dysfunction, and inhibiting glycogen synthase kinase 3 activity.

Flavonoids as detoxifying and pro-survival agents: What's new?

Flavonoids play a crucial role in cell survival and detoxification, but concerns remain about their biochemistry, bioavailability, pharmacokinetics, and gut microbiome interactions.

Tilianin Post-Conditioning Attenuates Myocardial Ischemia/Reperfusion Injury via Mitochondrial Protection and Inhibition of Apoptosis

Tilianin post-conditioning can reduce apoptosis and protect the heart during myocardial ischemia/reperfusion injury by protecting mitochondria and repressing mitochondrial apoptotic pathways.

Taxifolin protects RPE cells against oxidative stress-induced apoptosis

Taxifolin protects retinal pigment epithelial cells from oxidative stress-induced apoptosis by activating NRF2 and the phase II antioxidant enzyme system.

Citations

LncRNA 93358 Aggravates the Apoptosis of Myocardial Cells After Ischemia‐Reperfusion by Mediating the PI3K/AKT/mTOR Pathway

LncRNA 93358 aggravates myocardial cell apoptosis after ischemia-reperfusion by mediating the PI3K/AKT/mTOR pathway.

Unveiling the therapeutic potential of Taxifolin in Cancer: From molecular mechanisms to immune modulation and synergistic combinations.

Taxifolin shows promise as a versatile anticancer agent, offering direct anticancer effects and protective benefits against chemotherapy-induced toxicities.

Roles of flavonoids in ischemic heart disease: Cardioprotective effects and mechanisms against myocardial ischemia and reperfusion injury.

Flavonoids, found in fruits, vegetables, grains, and medicinal plants, show potential as cardioprotective agents against myocardial ischemia and reperfusion injuries through various mechanisms.

EFFECT OF TAXIFOLIN ON DOXORUBICIN-INDUCED OXIDATIVE CARDIAC DAMAGE IN RATS: A BIOCHEMICAL AND HISTOPATHOLOGICAL EVALUATION

Taxifolin may help treat doxorubicin-induced oxidative heart damage by inhibiting oxidative stress and reducing heart tissue damage markers.

Cardio-protective effects of Pinus eldarica bark extract on adrenaline-induced myocardial infarction in rats

Pinus eldarica bark extract shows cardioprotective and antioxidant effects against adrenaline-induced myocardial infarction, suggesting it as a potential treatment for this condition.

New Perspectives of Taxifolin in Neurodegenerative Diseases

Taxifolin shows potential in neurodegenerative diseases by suppressing inflammation, reducing oxidative stress, preventing A protein formation, maintaining dopamine levels, and reducing neuronal loss.

Cardioprotective Effect of Taxifolin against Isoproterenol-Induced Cardiac Injury through Decreasing Oxidative Stress, Inflammation, and Cell Death, and Activating Nrf2/HO-1 in Mice

Taxifolin protects against isoproterenol-induced acute myocardial injury by reducing oxidative stress, inflammation, and cell death, and activating the Nrf2/HO-1 signaling pathway in mice.

The effect of taxifolin on oxidative sciatic nerve damage induced by cobalt chloride in rats: a biochemical and histopathological evaluation.

Taxifolin effectively prevents cobalt-induced oxidative damage in sciatic nerve injury by reducing malondialdehyde levels and increasing antioxidant status.

Network Pharmacology-Based Combined with Experimental Validation Study to Explore the Underlying Mechanism of Agrimonia pilosa Ledeb. Extract in Treating Acute Myocardial Infarction

Agrimonia pilosa Ledeb. extract protects against acute myocardial infarction by reducing oxidative stress and apoptosis, potentially through activation of the PI3K/Akt signaling pathway.