Baicalin suppresses autophagy-dependent ferroptosis in early brain injury after subarachnoid hemorrhage

Early brain injury, characterized by massive cell apoptosis or death, is identified as a critical pathophysiological process during subarachnoid hemorrhage (SAH). Ferroptosis, a class of autophagy-dependent cell death discovered in 2012, is induced by iron-dependent lipid peroxidation accumulation....

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Autores principales:	Bao Zheng, Xiwei Zhou, Lujun Pang, Yanjun Che, Xin Qi
Formato:	article
Lenguaje:	EN
Publicado:	Taylor & Francis Group 2021
Materias:	baicalin ferroptosis brain injury sah Biotechnology TP248.13-248.65
Acceso en línea:	https://doaj.org/article/0af53fb41a2044ae8a03a8d8a74b5a2d
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spelling	oai:doaj.org-article:0af53fb41a2044ae8a03a8d8a74b5a2d2021-11-04T15:51:53ZBaicalin suppresses autophagy-dependent ferroptosis in early brain injury after subarachnoid hemorrhage2165-59792165-598710.1080/21655979.2021.1975999https://doaj.org/article/0af53fb41a2044ae8a03a8d8a74b5a2d2021-01-01T00:00:00Zhttp://dx.doi.org/10.1080/21655979.2021.1975999https://doaj.org/toc/2165-5979https://doaj.org/toc/2165-5987Early brain injury, characterized by massive cell apoptosis or death, is identified as a critical pathophysiological process during subarachnoid hemorrhage (SAH). Ferroptosis, a class of autophagy-dependent cell death discovered in 2012, is induced by iron-dependent lipid peroxidation accumulation. The present study was designed to study the role of baicalin in autophagy-dependent ferroptosis in early brain injury after SAH. Neurological scores and brain water content were measured to evaluate brain injury. Measurement of iron ion, malondialdehyde (MDA), lipid reactive oxygen species was conducted for ferroptosis evaluation. Immunofluorescence staining, western blotting, and flow cytometry analysis were used to evaluate autophagy and apoptosis. First, we observed that, compared with sham rats, SAH rats had lower neurobehavioral scores. Next, baicalin was proven to decrease the Fe2+, malondialdehyde, and ROS levels in the brain tissues of rats. Also, baicalin was confirmed to suppress the beclin1, LC3-II, and LC3-I protein levels in rat brain tissues. Moreover, we found that baicalin inhibited neuronal apoptosis. Finally, the effects of baicalin on brain injury in the SAH rats were verified. Overall, our results demonstrated that baicalin suppressed autophagy-dependent ferroptosis in EBI after SAH.Bao ZhengXiwei ZhouLujun PangYanjun CheXin QiTaylor & Francis Grouparticlebaicalinferroptosisbrain injurysahBiotechnologyTP248.13-248.65ENBioengineered, Vol 12, Iss 1, Pp 7794-7804 (2021)
institution	DOAJ
collection	DOAJ
language	EN
topic	baicalin ferroptosis brain injury sah Biotechnology TP248.13-248.65
spellingShingle	baicalin ferroptosis brain injury sah Biotechnology TP248.13-248.65 Bao Zheng Xiwei Zhou Lujun Pang Yanjun Che Xin Qi Baicalin suppresses autophagy-dependent ferroptosis in early brain injury after subarachnoid hemorrhage
description	Early brain injury, characterized by massive cell apoptosis or death, is identified as a critical pathophysiological process during subarachnoid hemorrhage (SAH). Ferroptosis, a class of autophagy-dependent cell death discovered in 2012, is induced by iron-dependent lipid peroxidation accumulation. The present study was designed to study the role of baicalin in autophagy-dependent ferroptosis in early brain injury after SAH. Neurological scores and brain water content were measured to evaluate brain injury. Measurement of iron ion, malondialdehyde (MDA), lipid reactive oxygen species was conducted for ferroptosis evaluation. Immunofluorescence staining, western blotting, and flow cytometry analysis were used to evaluate autophagy and apoptosis. First, we observed that, compared with sham rats, SAH rats had lower neurobehavioral scores. Next, baicalin was proven to decrease the Fe2+, malondialdehyde, and ROS levels in the brain tissues of rats. Also, baicalin was confirmed to suppress the beclin1, LC3-II, and LC3-I protein levels in rat brain tissues. Moreover, we found that baicalin inhibited neuronal apoptosis. Finally, the effects of baicalin on brain injury in the SAH rats were verified. Overall, our results demonstrated that baicalin suppressed autophagy-dependent ferroptosis in EBI after SAH.
format	article
author	Bao Zheng Xiwei Zhou Lujun Pang Yanjun Che Xin Qi
author_facet	Bao Zheng Xiwei Zhou Lujun Pang Yanjun Che Xin Qi
author_sort	Bao Zheng
title	Baicalin suppresses autophagy-dependent ferroptosis in early brain injury after subarachnoid hemorrhage
title_short	Baicalin suppresses autophagy-dependent ferroptosis in early brain injury after subarachnoid hemorrhage
title_full	Baicalin suppresses autophagy-dependent ferroptosis in early brain injury after subarachnoid hemorrhage
title_fullStr	Baicalin suppresses autophagy-dependent ferroptosis in early brain injury after subarachnoid hemorrhage
title_full_unstemmed	Baicalin suppresses autophagy-dependent ferroptosis in early brain injury after subarachnoid hemorrhage
title_sort	baicalin suppresses autophagy-dependent ferroptosis in early brain injury after subarachnoid hemorrhage
publisher	Taylor & Francis Group
publishDate	2021
url	https://doaj.org/article/0af53fb41a2044ae8a03a8d8a74b5a2d
work_keys_str_mv	AT baozheng baicalinsuppressesautophagydependentferroptosisinearlybraininjuryaftersubarachnoidhemorrhage AT xiweizhou baicalinsuppressesautophagydependentferroptosisinearlybraininjuryaftersubarachnoidhemorrhage AT lujunpang baicalinsuppressesautophagydependentferroptosisinearlybraininjuryaftersubarachnoidhemorrhage AT yanjunche baicalinsuppressesautophagydependentferroptosisinearlybraininjuryaftersubarachnoidhemorrhage AT xinqi baicalinsuppressesautophagydependentferroptosisinearlybraininjuryaftersubarachnoidhemorrhage
_version_	1718444694049914880

Baicalin suppresses autophagy-dependent ferroptosis in early brain injury after subarachnoid hemorrhage

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