Targeting Oxidative Stress and Inflammatory Response for Blood-Brain Barrier Protection in Intracerebral Hemorrhage

Blood-brain barrier (BBB) disruption is a major pathological change after intracerebral hemorrhage (ICH) and is both the cause and result of oxidative stress and of the immune response post-ICH. These processes contribute to ICH-induced brain injury. After the breakdown of cerebral vessels, blood co...

Ausführliche Beschreibung

Gespeichert in:
Bibliographische Detailangaben
Veröffentlicht in:Antioxidants & redox signaling Jg. 37; H. 1-3; S. 115
Hauptverfasser: Chen, Shengpan, Li, Lingzhi, Peng, Chao, Bian, Chunjing, Ocak, Pinar Eser, Zhang, John H, Yang, Yong, Zhou, Dong, Chen, Guangzhong, Luo, Yumin
Format: Journal Article
Sprache:Englisch
Veröffentlicht: United States 01.07.2022
Schlagworte:
ISSN:1557-7716, 1557-7716
Online-Zugang:Weitere Angaben
Tags: Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
Abstract Blood-brain barrier (BBB) disruption is a major pathological change after intracerebral hemorrhage (ICH) and is both the cause and result of oxidative stress and of the immune response post-ICH. These processes contribute to ICH-induced brain injury. After the breakdown of cerebral vessels, blood components, including erythrocytes and their metabolites, thrombin, and fibrinogen, can access the cerebral parenchyma through the compromised BBB, triggering oxidative stress and inflammatory cascades. These aggravate BBB disruption and contribute to further infiltration of blood components, resulting in a vicious cycle that exacerbates brain edema and neurological injury after ICH. Experimental and clinical studies have highlighted the role of BBB disruption in ICH-induced brain injury. In this review, we focus on the strategies to protect the BBB in ICH. Specifically, we summarize the evidence and the underlying mechanisms, including the ICH-induced process of oxidative stress and inflammatory response, and we highlight the potential therapeutic targets to protect BBB integrity after ICH. Future studies should probe the mechanism of ferroptosis as well as oxidative stress-inflammation coupling in BBB disruption after ICH and investigate the effects of antioxidants and immunomodulatory agents in more ICH clinical trials.
AbstractList Blood-brain barrier (BBB) disruption is a major pathological change after intracerebral hemorrhage (ICH) and is both the cause and result of oxidative stress and of the immune response post-ICH. These processes contribute to ICH-induced brain injury. After the breakdown of cerebral vessels, blood components, including erythrocytes and their metabolites, thrombin, and fibrinogen, can access the cerebral parenchyma through the compromised BBB, triggering oxidative stress and inflammatory cascades. These aggravate BBB disruption and contribute to further infiltration of blood components, resulting in a vicious cycle that exacerbates brain edema and neurological injury after ICH. Experimental and clinical studies have highlighted the role of BBB disruption in ICH-induced brain injury. In this review, we focus on the strategies to protect the BBB in ICH. Specifically, we summarize the evidence and the underlying mechanisms, including the ICH-induced process of oxidative stress and inflammatory response, and we highlight the potential therapeutic targets to protect BBB integrity after ICH. Future studies should probe the mechanism of ferroptosis as well as oxidative stress-inflammation coupling in BBB disruption after ICH and investigate the effects of antioxidants and immunomodulatory agents in more ICH clinical trials.
Significance: Blood-brain barrier (BBB) disruption is a major pathological change after intracerebral hemorrhage (ICH) and is both the cause and result of oxidative stress and of the immune response post-ICH. These processes contribute to ICH-induced brain injury. Recent Advances: After the breakdown of cerebral vessels, blood components, including erythrocytes and their metabolites, thrombin, and fibrinogen, can access the cerebral parenchyma through the compromised BBB, triggering oxidative stress and inflammatory cascades. These aggravate BBB disruption and contribute to further infiltration of blood components, resulting in a vicious cycle that exacerbates brain edema and neurological injury after ICH. Experimental and clinical studies have highlighted the role of BBB disruption in ICH-induced brain injury. Critical Issues: In this review, we focus on the strategies to protect the BBB in ICH. Specifically, we summarize the evidence and the underlying mechanisms, including the ICH-induced process of oxidative stress and inflammatory response, and we highlight the potential therapeutic targets to protect BBB integrity after ICH. Future Directions: Future studies should probe the mechanism of ferroptosis as well as oxidative stress-inflammation coupling in BBB disruption after ICH and investigate the effects of antioxidants and immunomodulatory agents in more ICH clinical trials. Antioxid. Redox Signal. 37, 115-134.Significance: Blood-brain barrier (BBB) disruption is a major pathological change after intracerebral hemorrhage (ICH) and is both the cause and result of oxidative stress and of the immune response post-ICH. These processes contribute to ICH-induced brain injury. Recent Advances: After the breakdown of cerebral vessels, blood components, including erythrocytes and their metabolites, thrombin, and fibrinogen, can access the cerebral parenchyma through the compromised BBB, triggering oxidative stress and inflammatory cascades. These aggravate BBB disruption and contribute to further infiltration of blood components, resulting in a vicious cycle that exacerbates brain edema and neurological injury after ICH. Experimental and clinical studies have highlighted the role of BBB disruption in ICH-induced brain injury. Critical Issues: In this review, we focus on the strategies to protect the BBB in ICH. Specifically, we summarize the evidence and the underlying mechanisms, including the ICH-induced process of oxidative stress and inflammatory response, and we highlight the potential therapeutic targets to protect BBB integrity after ICH. Future Directions: Future studies should probe the mechanism of ferroptosis as well as oxidative stress-inflammation coupling in BBB disruption after ICH and investigate the effects of antioxidants and immunomodulatory agents in more ICH clinical trials. Antioxid. Redox Signal. 37, 115-134.
Author Bian, Chunjing
Chen, Shengpan
Li, Lingzhi
Zhang, John H
Peng, Chao
Chen, Guangzhong
Luo, Yumin
Ocak, Pinar Eser
Yang, Yong
Zhou, Dong
Author_xml – sequence: 1
  givenname: Shengpan
  orcidid: 0000-0002-0164-1980
  surname: Chen
  fullname: Chen, Shengpan
  organization: Department of Neurosurgery, Guangdong Provincial People's Hospital, Guangdong Institute of Neuroscience, Guangdong Academy of Medical Sciences, Guangzhou, China
– sequence: 2
  givenname: Lingzhi
  surname: Li
  fullname: Li, Lingzhi
  organization: Institute of Cerebrovascular Disease Research and Department of Neurology, Xuanwu Hospital of Capital Medical University, Beijing, China
– sequence: 3
  givenname: Chao
  surname: Peng
  fullname: Peng, Chao
  organization: Department of Neurosurgery, Guangdong Provincial People's Hospital, Guangdong Institute of Neuroscience, Guangdong Academy of Medical Sciences, Guangzhou, China
– sequence: 4
  givenname: Chunjing
  surname: Bian
  fullname: Bian, Chunjing
  organization: Department of General Surgery, Xuanwu Hospital, Capital Medical University, Beijing, China
– sequence: 5
  givenname: Pinar Eser
  surname: Ocak
  fullname: Ocak, Pinar Eser
  organization: Department of Neurosurgery, Uludag University School of Medicine, Bursa, Turkey
– sequence: 6
  givenname: John H
  surname: Zhang
  fullname: Zhang, John H
  organization: Department of Neurosurgery, Loma Linda University, Loma Linda, California, USA
– sequence: 7
  givenname: Yong
  surname: Yang
  fullname: Yang, Yong
  organization: Department of Neurosurgery, Guangdong Provincial People's Hospital, Guangdong Institute of Neuroscience, Guangdong Academy of Medical Sciences, Guangzhou, China
– sequence: 8
  givenname: Dong
  surname: Zhou
  fullname: Zhou, Dong
  organization: Department of Neurosurgery, Guangdong Provincial People's Hospital, Guangdong Institute of Neuroscience, Guangdong Academy of Medical Sciences, Guangzhou, China
– sequence: 9
  givenname: Guangzhong
  surname: Chen
  fullname: Chen, Guangzhong
  organization: Department of Neurosurgery, Guangdong Provincial People's Hospital, Guangdong Institute of Neuroscience, Guangdong Academy of Medical Sciences, Guangzhou, China
– sequence: 10
  givenname: Yumin
  surname: Luo
  fullname: Luo, Yumin
  organization: Beijing Geriatric Medical Research Center and Beijing Key Laboratory of Translational Medicine for Cerebrovascular Diseases, Beijing, China
BackLink https://www.ncbi.nlm.nih.gov/pubmed/35383484$$D View this record in MEDLINE/PubMed
BookMark eNpNkEtPAjEUhRuDkYcu3Zou3Qz2MZ2WpRAVEhKM4ppcZi44ZqbF22Lk30siJq7Ol5MvZ3H6rOODR8aupRhK4UZ3QHGohJJDIaw6Yz1pjM2slUXnH3dZP8YPIY6eFBesq412Ond5j8Ul0BZT7bd88V1XkOov5K-JMEYOvuIzv2mgbSEFOvAXjLvgI_JNID5uQqiyMUHt-RiIaiT-TCFhmerg-bGd-URQIuGaoOFTbAPRO2zxkp1voIl4dcoBe3t8WE6m2XzxNJvcz7NSmyJlRq_FSDoU1uRYQq6s2xgjAFRRjYxEWRZr5dBoHDlw0gqFuQZnReUqlxeoBuz2d3dH4XOPMa3aOpbYNOAx7ONKFbktjNZCHdWbk7pft1itdlS3QIfV31HqB0VsbOU
CitedBy_id crossref_primary_10_3390_diagnostics14222561
crossref_primary_10_1016_j_intimp_2023_110744
crossref_primary_10_1186_s12938_024_01288_y
crossref_primary_10_1016_j_intimp_2024_112049
crossref_primary_10_1016_j_intimp_2025_114945
crossref_primary_10_3390_antiox14060692
crossref_primary_10_1016_j_neuroscience_2025_08_050
crossref_primary_10_2147_DDDT_S439873
crossref_primary_10_3389_fnins_2024_1413483
crossref_primary_10_1016_j_clineuro_2024_108287
crossref_primary_10_3389_fmed_2025_1578666
crossref_primary_10_1016_j_biochi_2024_03_015
crossref_primary_10_1016_j_cej_2024_158069
crossref_primary_10_1002_brb3_70507
crossref_primary_10_1016_j_imlet_2023_11_002
crossref_primary_10_1016_j_neuropharm_2025_110538
crossref_primary_10_1073_pnas_2417224122
crossref_primary_10_1007_s12975_023_01225_6
crossref_primary_10_1007_s40618_025_02603_7
crossref_primary_10_31083_j_jin2205113
crossref_primary_10_1515_nanoph_2022_0496
crossref_primary_10_3389_fnins_2024_1517601
crossref_primary_10_1007_s12033_023_00882_0
crossref_primary_10_1007_s12975_025_01341_5
crossref_primary_10_1186_s12987_024_00563_3
crossref_primary_10_3389_fcell_2023_1142923
crossref_primary_10_1016_j_prp_2024_155705
crossref_primary_10_3389_fphar_2024_1293428
crossref_primary_10_1186_s12987_023_00434_3
crossref_primary_10_1016_j_jep_2023_116298
crossref_primary_10_1007_s11010_024_05150_6
crossref_primary_10_3390_ijms23115913
crossref_primary_10_1016_j_mito_2023_01_007
crossref_primary_10_1080_0886022X_2023_2259234
crossref_primary_10_1016_j_actbio_2024_03_023
crossref_primary_10_1016_j_brainresbull_2024_111153
crossref_primary_10_2147_IJGM_S457480
crossref_primary_10_1016_j_hest_2024_10_001
crossref_primary_10_1097_WNR_0000000000002026
crossref_primary_10_1111_cns_14255
crossref_primary_10_1016_j_cbpc_2025_110164
crossref_primary_10_1016_j_ejphar_2023_176105
crossref_primary_10_1111_cns_14853
crossref_primary_10_1007_s13273_023_00397_4
crossref_primary_10_3389_fncel_2023_1298314
crossref_primary_10_3390_cells13191635
crossref_primary_10_1016_j_expneurol_2024_115036
crossref_primary_10_1039_D3FO03568A
crossref_primary_10_3233_JAD_220700
crossref_primary_10_3389_fneur_2024_1510039
crossref_primary_10_3389_fneur_2025_1533558
crossref_primary_10_3389_fneur_2023_1077518
crossref_primary_10_3389_fneur_2023_1234252
crossref_primary_10_1007_s12035_023_03643_x
crossref_primary_10_1007_s11064_023_03892_1
crossref_primary_10_1016_j_expneurol_2024_114948
crossref_primary_10_3389_fnagi_2025_1627353
crossref_primary_10_1007_s12035_025_04886_6
crossref_primary_10_1097_WNR_0000000000002180
crossref_primary_10_2147_JIR_S411017
crossref_primary_10_2147_JIR_S498809
crossref_primary_10_1016_j_heliyon_2023_e17874
crossref_primary_10_3389_fendo_2023_1290176
crossref_primary_10_1016_j_bbrc_2023_03_007
crossref_primary_10_1016_j_jare_2024_11_008
crossref_primary_10_1016_j_jns_2025_123534
crossref_primary_10_1177_09603271231184630
crossref_primary_10_3390_ijms251910321
crossref_primary_10_3389_fneur_2025_1578975
crossref_primary_10_1016_j_brainres_2023_148373
crossref_primary_10_31083_j_jin2205134
crossref_primary_10_4103_NRR_NRR_D_23_01889
crossref_primary_10_1007_s12975_025_01342_4
crossref_primary_10_1016_j_jnrt_2025_100230
crossref_primary_10_1016_j_freeradbiomed_2024_03_019
crossref_primary_10_1002_brb3_70493
crossref_primary_10_2147_DDDT_S513343
crossref_primary_10_3389_fneur_2024_1337168
crossref_primary_10_12677_acm_2025_1561711
crossref_primary_10_1007_s12975_024_01240_1
crossref_primary_10_1016_j_intimp_2024_111962
crossref_primary_10_3389_fnbeh_2022_912896
crossref_primary_10_1002_jat_4614
crossref_primary_10_1016_j_intimp_2024_112774
crossref_primary_10_1016_j_lssr_2024_08_001
crossref_primary_10_3389_fnagi_2024_1365086
crossref_primary_10_1016_j_intimp_2023_110698
crossref_primary_10_1016_j_wneu_2024_03_107
crossref_primary_10_3389_fnagi_2022_1024496
crossref_primary_10_3389_fphar_2024_1360932
crossref_primary_10_3389_fneur_2023_1288377
crossref_primary_10_1007_s11033_024_09952_1
crossref_primary_10_1016_j_apsb_2025_07_014
crossref_primary_10_1016_j_colsurfb_2024_113857
crossref_primary_10_1016_j_jes_2025_06_002
crossref_primary_10_3390_ijms26062781
ContentType Journal Article
DBID NPM
7X8
DOI 10.1089/ars.2021.0072
DatabaseName PubMed
MEDLINE - Academic
DatabaseTitle PubMed
MEDLINE - Academic
DatabaseTitleList PubMed
MEDLINE - Academic
Database_xml – sequence: 1
  dbid: NPM
  name: PubMed
  url: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed
  sourceTypes: Index Database
– sequence: 2
  dbid: 7X8
  name: MEDLINE - Academic
  url: https://search.proquest.com/medline
  sourceTypes: Aggregation Database
DeliveryMethod no_fulltext_linktorsrc
Discipline Medicine
Chemistry
EISSN 1557-7716
ExternalDocumentID 35383484
Genre Journal Article
GroupedDBID ---
0R~
23M
4.4
5GY
5RE
ABBKN
ABJNI
ACGFS
ACPRK
ADBBV
AENEX
AFOSN
AFRAH
ALMA_UNASSIGNED_HOLDINGS
BNQNF
CS3
EBS
F5P
IER
IHR
IM4
MV1
NPM
NQHIM
O9-
P2P
RML
UE5
7X8
SCNPE
ID FETCH-LOGICAL-c356t-53b0918e0754eca4278f550aa26d951e1c6b28e53e98a81702e43a870d8d846e2
IEDL.DBID 7X8
ISICitedReferencesCount 130
ISICitedReferencesURI http://www.webofscience.com/api/gateway?GWVersion=2&SrcApp=Summon&SrcAuth=ProQuest&DestLinkType=CitingArticles&DestApp=WOS_CPL&KeyUT=000807966200001&url=https%3A%2F%2Fcvtisr.summon.serialssolutions.com%2F%23%21%2Fsearch%3Fho%3Df%26include.ft.matches%3Dt%26l%3Dnull%26q%3D
ISSN 1557-7716
IngestDate Thu Sep 04 17:55:15 EDT 2025
Thu Jan 02 22:53:59 EST 2025
IsPeerReviewed true
IsScholarly true
Issue 1-3
Keywords intracerebral hemorrhage
inflammatory response
blood–brain barrier
blood components
oxidative stress
Language English
LinkModel DirectLink
MergedId FETCHMERGED-LOGICAL-c356t-53b0918e0754eca4278f550aa26d951e1c6b28e53e98a81702e43a870d8d846e2
Notes ObjectType-Article-1
SourceType-Scholarly Journals-1
ObjectType-Feature-2
ObjectType-Review-3
content type line 23
ORCID 0000-0002-0164-1980
PMID 35383484
PQID 2647653302
PQPubID 23479
ParticipantIDs proquest_miscellaneous_2647653302
pubmed_primary_35383484
PublicationCentury 2000
PublicationDate 2022-07-01
PublicationDateYYYYMMDD 2022-07-01
PublicationDate_xml – month: 07
  year: 2022
  text: 2022-07-01
  day: 01
PublicationDecade 2020
PublicationPlace United States
PublicationPlace_xml – name: United States
PublicationTitle Antioxidants & redox signaling
PublicationTitleAlternate Antioxid Redox Signal
PublicationYear 2022
SSID ssj0002110
Score 2.657532
SecondaryResourceType review_article
Snippet Blood-brain barrier (BBB) disruption is a major pathological change after intracerebral hemorrhage (ICH) and is both the cause and result of oxidative stress...
Significance: Blood-brain barrier (BBB) disruption is a major pathological change after intracerebral hemorrhage (ICH) and is both the cause and result of...
SourceID proquest
pubmed
SourceType Aggregation Database
Index Database
StartPage 115
Title Targeting Oxidative Stress and Inflammatory Response for Blood-Brain Barrier Protection in Intracerebral Hemorrhage
URI https://www.ncbi.nlm.nih.gov/pubmed/35383484
https://www.proquest.com/docview/2647653302
Volume 37
WOSCitedRecordID wos000807966200001&url=https%3A%2F%2Fcvtisr.summon.serialssolutions.com%2F%23%21%2Fsearch%3Fho%3Df%26include.ft.matches%3Dt%26l%3Dnull%26q%3D
hasFullText
inHoldings 1
isFullTextHit
isPrint
link http://cvtisr.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwpV1LS8NAEF7UinrxUV_1xQpeg81uniexxdIeWotW6K3sYxYLmtakij_f2U1KT4LgJYeQQNjdzHyz8-33EXLTZMBSI43Hoph5gdFNT8pUenFoNEsiROSgnNlEPBgk43E6rDbciopWuYyJLlDrmbJ75LeYuOPIUiHZ3fzDs65RtrtaWWiskxpHKGMpXfF4pRZuixunlxrGiCL9qNLYbCbpLVaNWBwy30ln_44uXZbp7P33-_bJboUv6X25IA7IGmR1st1e2rrVyVa_6qYfkmLkaOCYvOjj91Q7CXD67A6PUJFp2ssMrpd314enTyWZFiiiXNpydPeWtZegLZFb1zs6LBUfcJ4p3u3ZTWMFue1Lv9Gu5fPmrxi7jshL52HU7nqVCYOneBgtvJBLhBQJILQIQAnrzGGwqhGCRRrRGfgqkiyBkEOaCKv2xyDgAqOATjRiG2DHZCObZXBKaMAkors4ljzSgZS-NJhC7VOKB1r60CDXy6Gd4KDYzoXIYPZZTFaD2yAn5fxM5qUax4RjyOZBEpz94e1zssPs8QVHt70gNYO_OFySTfW1mBb5lVs9eB0M-z88K8_o
linkProvider ProQuest
openUrl ctx_ver=Z39.88-2004&ctx_enc=info%3Aofi%2Fenc%3AUTF-8&rfr_id=info%3Asid%2Fsummon.serialssolutions.com&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.genre=article&rft.atitle=Targeting+Oxidative+Stress+and+Inflammatory+Response+for+Blood-Brain+Barrier+Protection+in+Intracerebral+Hemorrhage&rft.jtitle=Antioxidants+%26+redox+signaling&rft.au=Chen%2C+Shengpan&rft.au=Li%2C+Lingzhi&rft.au=Peng%2C+Chao&rft.au=Bian%2C+Chunjing&rft.date=2022-07-01&rft.eissn=1557-7716&rft_id=info:doi/10.1089%2Fars.2021.0072&rft_id=info%3Apmid%2F35383484&rft_id=info%3Apmid%2F35383484&rft.externalDocID=35383484
thumbnail_l http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/lc.gif&issn=1557-7716&client=summon
thumbnail_m http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/mc.gif&issn=1557-7716&client=summon
thumbnail_s http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/sc.gif&issn=1557-7716&client=summon