Baicalin Prevents Myocardial Ischemia/Reperfusion Injury Through Inhibiting ACSL4 Mediated Ferroptosis
Baicalin is a natural flavonoid glycoside that confers protection against myocardial ischemia/reperfusion (I/R) injury. However, its mechanism has not been fully understood. This study focused on elucidating the role of ferroptosis in baicalin-generated protective effects on myocardial ischemia/repe...
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2021-04-01
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doaj-84729df243a44dcd98f7f419671aa1c82021-04-14T05:54:17ZengFrontiers Media S.A.Frontiers in Pharmacology1663-98122021-04-011210.3389/fphar.2021.628988628988Baicalin Prevents Myocardial Ischemia/Reperfusion Injury Through Inhibiting ACSL4 Mediated FerroptosisZhenyu FanLiangliang CaiShengnan WangJing WangBohua ChenBaicalin is a natural flavonoid glycoside that confers protection against myocardial ischemia/reperfusion (I/R) injury. However, its mechanism has not been fully understood. This study focused on elucidating the role of ferroptosis in baicalin-generated protective effects on myocardial ischemia/reperfusion (I/R) injury by using the myocardial I/R rat model and oxygen–glucose deprivation/reoxygenation (OGD/R) H9c2 cells. Our results show that baicalin improved myocardial I/R challenge–induced ST segment elevation, coronary flow (CF), left ventricular systolic pressure , infarct area, and pathological changes and prevented OGD/R-triggered cell viability loss. In addition, enhanced lipid peroxidation and significant iron accumulation along with activated transferrin receptor protein 1 (TfR1) signal and nuclear receptor coactivator 4 (NCOA4)-medicated ferritinophagy were observed in in vivo and in vitro models, which were reversed by baicalin treatment. Furthermore, acyl-CoA synthetase long-chain family member 4 (ACSL4) overexpression compromised baicalin-generated protective effect in H9c2 cells. Taken together, our findings suggest that baicalin prevents against myocardial ischemia/reperfusion injury via suppressing ACSL4-controlled ferroptosis. This study provides a novel target for the prevention of myocardial ischemia/reperfusion injury.https://www.frontiersin.org/articles/10.3389/fphar.2021.628988/fullbaicalinferroptosisacyl-CoA synthetase long-chain family member 4myocardialischemia/reperfusion injury |
collection |
DOAJ |
language |
English |
format |
Article |
sources |
DOAJ |
author |
Zhenyu Fan Liangliang Cai Shengnan Wang Jing Wang Bohua Chen |
spellingShingle |
Zhenyu Fan Liangliang Cai Shengnan Wang Jing Wang Bohua Chen Baicalin Prevents Myocardial Ischemia/Reperfusion Injury Through Inhibiting ACSL4 Mediated Ferroptosis Frontiers in Pharmacology baicalin ferroptosis acyl-CoA synthetase long-chain family member 4 myocardial ischemia/reperfusion injury |
author_facet |
Zhenyu Fan Liangliang Cai Shengnan Wang Jing Wang Bohua Chen |
author_sort |
Zhenyu Fan |
title |
Baicalin Prevents Myocardial Ischemia/Reperfusion Injury Through Inhibiting ACSL4 Mediated Ferroptosis |
title_short |
Baicalin Prevents Myocardial Ischemia/Reperfusion Injury Through Inhibiting ACSL4 Mediated Ferroptosis |
title_full |
Baicalin Prevents Myocardial Ischemia/Reperfusion Injury Through Inhibiting ACSL4 Mediated Ferroptosis |
title_fullStr |
Baicalin Prevents Myocardial Ischemia/Reperfusion Injury Through Inhibiting ACSL4 Mediated Ferroptosis |
title_full_unstemmed |
Baicalin Prevents Myocardial Ischemia/Reperfusion Injury Through Inhibiting ACSL4 Mediated Ferroptosis |
title_sort |
baicalin prevents myocardial ischemia/reperfusion injury through inhibiting acsl4 mediated ferroptosis |
publisher |
Frontiers Media S.A. |
series |
Frontiers in Pharmacology |
issn |
1663-9812 |
publishDate |
2021-04-01 |
description |
Baicalin is a natural flavonoid glycoside that confers protection against myocardial ischemia/reperfusion (I/R) injury. However, its mechanism has not been fully understood. This study focused on elucidating the role of ferroptosis in baicalin-generated protective effects on myocardial ischemia/reperfusion (I/R) injury by using the myocardial I/R rat model and oxygen–glucose deprivation/reoxygenation (OGD/R) H9c2 cells. Our results show that baicalin improved myocardial I/R challenge–induced ST segment elevation, coronary flow (CF), left ventricular systolic pressure , infarct area, and pathological changes and prevented OGD/R-triggered cell viability loss. In addition, enhanced lipid peroxidation and significant iron accumulation along with activated transferrin receptor protein 1 (TfR1) signal and nuclear receptor coactivator 4 (NCOA4)-medicated ferritinophagy were observed in in vivo and in vitro models, which were reversed by baicalin treatment. Furthermore, acyl-CoA synthetase long-chain family member 4 (ACSL4) overexpression compromised baicalin-generated protective effect in H9c2 cells. Taken together, our findings suggest that baicalin prevents against myocardial ischemia/reperfusion injury via suppressing ACSL4-controlled ferroptosis. This study provides a novel target for the prevention of myocardial ischemia/reperfusion injury. |
topic |
baicalin ferroptosis acyl-CoA synthetase long-chain family member 4 myocardial ischemia/reperfusion injury |
url |
https://www.frontiersin.org/articles/10.3389/fphar.2021.628988/full |
work_keys_str_mv |
AT zhenyufan baicalinpreventsmyocardialischemiareperfusioninjurythroughinhibitingacsl4mediatedferroptosis AT liangliangcai baicalinpreventsmyocardialischemiareperfusioninjurythroughinhibitingacsl4mediatedferroptosis AT shengnanwang baicalinpreventsmyocardialischemiareperfusioninjurythroughinhibitingacsl4mediatedferroptosis AT jingwang baicalinpreventsmyocardialischemiareperfusioninjurythroughinhibitingacsl4mediatedferroptosis AT bohuachen baicalinpreventsmyocardialischemiareperfusioninjurythroughinhibitingacsl4mediatedferroptosis |
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1721527654781288448 |