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...
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| Veröffentlicht in: | Antioxidants & redox signaling Jg. 37; H. 1-3; S. 115 |
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01.07.2022
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| 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. |
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| 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 |
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| Title | Targeting Oxidative Stress and Inflammatory Response for Blood-Brain Barrier Protection in Intracerebral Hemorrhage |
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