Role of NADPH oxidase in the brain injury of intracerebral hemorrhage
The major risk factors for intracerebral hemorrhage (ICH) are hypertension and aging. A fundamental mechanism for hypertension- and aging-induced vascular injury is oxidative stress. We hypothesize that oxidative stress has a crucial role in ICH. To test our hypothesis, we used bacterial collagenase...
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| Autor*in: |
Tang, Jiping [verfasserIn] Liu, Jun [verfasserIn] Zhou, Changman [verfasserIn] |
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| Format: |
E-Artikel |
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| Erschienen: |
Oxford, UK: Blackwell Science Ltd ; 2005 |
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| Umfang: |
Online-Ressource |
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2005 ; Blackwell Publishing Journal Backfiles 1879-2005 |
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In: Journal of neurochemistry - Oxford : Wiley-Blackwell, 1956, 94(2005), 5, Seite 0 |
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volume:94 ; year:2005 ; number:5 ; pages:0 |
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| DOI / URN: |
10.1111/j.1471-4159.2005.03292.x |
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| 520 | |a The major risk factors for intracerebral hemorrhage (ICH) are hypertension and aging. A fundamental mechanism for hypertension- and aging-induced vascular injury is oxidative stress. We hypothesize that oxidative stress has a crucial role in ICH. To test our hypothesis, we used bacterial collagenase to produce ICH in wild-type C57BL/6 and gp91phox knockout (gp91phox KO) mice (deficient in gp91phox subunit of the superoxide-producing enzyme NADPH oxidase). All animals were studied at 20–35 weeks of age, resembling an older patient population. We found that collagenase produced less bleeding in gp91phox KO mice than wild-type mice. Total oxidative product was lower in gp91phox KO mice than in wild-type mice, both under basal conditions and after ICH. Consistent with the ICH volume, brain edema formation, neurological deficit and a high mortality rate was noted in wild-type but not in gp91phox KO mice. This ICH-induced brain injury in wild-type mice is associated with enhanced expression of the gp91phox subunit of NADPH oxidase. In conclusion, the oxidative stress resulting from activation of NADPH oxidase contributes to ICH induced by collagenase and promotes brain injury. | ||
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10.1111/j.1471-4159.2005.03292.x doi (DE-627)NLEJ243113226 DE-627 ger DE-627 rakwb Tang, Jiping verfasserin aut Role of NADPH oxidase in the brain injury of intracerebral hemorrhage Oxford, UK Blackwell Science Ltd 2005 Online-Ressource nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier The major risk factors for intracerebral hemorrhage (ICH) are hypertension and aging. A fundamental mechanism for hypertension- and aging-induced vascular injury is oxidative stress. We hypothesize that oxidative stress has a crucial role in ICH. To test our hypothesis, we used bacterial collagenase to produce ICH in wild-type C57BL/6 and gp91phox knockout (gp91phox KO) mice (deficient in gp91phox subunit of the superoxide-producing enzyme NADPH oxidase). All animals were studied at 20–35 weeks of age, resembling an older patient population. We found that collagenase produced less bleeding in gp91phox KO mice than wild-type mice. Total oxidative product was lower in gp91phox KO mice than in wild-type mice, both under basal conditions and after ICH. Consistent with the ICH volume, brain edema formation, neurological deficit and a high mortality rate was noted in wild-type but not in gp91phox KO mice. This ICH-induced brain injury in wild-type mice is associated with enhanced expression of the gp91phox subunit of NADPH oxidase. In conclusion, the oxidative stress resulting from activation of NADPH oxidase contributes to ICH induced by collagenase and promotes brain injury. 2005 Blackwell Publishing Journal Backfiles 1879-2005 |2005|||||||||| collagenase Liu, Jun verfasserin aut Zhou, Changman verfasserin aut Ostanin, Dmitry oth Grisham, Matthew B. oth Neil Granger, D. oth Zhang, John H. oth In Journal of neurochemistry Oxford : Wiley-Blackwell, 1956 94(2005), 5, Seite 0 Online-Ressource (DE-627)NLEJ243927584 (DE-600)2020528-4 1471-4159 nnns volume:94 year:2005 number:5 pages:0 http://dx.doi.org/10.1111/j.1471-4159.2005.03292.x text/html Verlag Deutschlandweit zugänglich Volltext GBV_USEFLAG_U ZDB-1-DJB GBV_NL_ARTICLE AR 94 2005 5 0 |
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10.1111/j.1471-4159.2005.03292.x doi (DE-627)NLEJ243113226 DE-627 ger DE-627 rakwb Tang, Jiping verfasserin aut Role of NADPH oxidase in the brain injury of intracerebral hemorrhage Oxford, UK Blackwell Science Ltd 2005 Online-Ressource nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier The major risk factors for intracerebral hemorrhage (ICH) are hypertension and aging. A fundamental mechanism for hypertension- and aging-induced vascular injury is oxidative stress. We hypothesize that oxidative stress has a crucial role in ICH. To test our hypothesis, we used bacterial collagenase to produce ICH in wild-type C57BL/6 and gp91phox knockout (gp91phox KO) mice (deficient in gp91phox subunit of the superoxide-producing enzyme NADPH oxidase). All animals were studied at 20–35 weeks of age, resembling an older patient population. We found that collagenase produced less bleeding in gp91phox KO mice than wild-type mice. Total oxidative product was lower in gp91phox KO mice than in wild-type mice, both under basal conditions and after ICH. Consistent with the ICH volume, brain edema formation, neurological deficit and a high mortality rate was noted in wild-type but not in gp91phox KO mice. This ICH-induced brain injury in wild-type mice is associated with enhanced expression of the gp91phox subunit of NADPH oxidase. In conclusion, the oxidative stress resulting from activation of NADPH oxidase contributes to ICH induced by collagenase and promotes brain injury. 2005 Blackwell Publishing Journal Backfiles 1879-2005 |2005|||||||||| collagenase Liu, Jun verfasserin aut Zhou, Changman verfasserin aut Ostanin, Dmitry oth Grisham, Matthew B. oth Neil Granger, D. oth Zhang, John H. oth In Journal of neurochemistry Oxford : Wiley-Blackwell, 1956 94(2005), 5, Seite 0 Online-Ressource (DE-627)NLEJ243927584 (DE-600)2020528-4 1471-4159 nnns volume:94 year:2005 number:5 pages:0 http://dx.doi.org/10.1111/j.1471-4159.2005.03292.x text/html Verlag Deutschlandweit zugänglich Volltext GBV_USEFLAG_U ZDB-1-DJB GBV_NL_ARTICLE AR 94 2005 5 0 |
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10.1111/j.1471-4159.2005.03292.x doi (DE-627)NLEJ243113226 DE-627 ger DE-627 rakwb Tang, Jiping verfasserin aut Role of NADPH oxidase in the brain injury of intracerebral hemorrhage Oxford, UK Blackwell Science Ltd 2005 Online-Ressource nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier The major risk factors for intracerebral hemorrhage (ICH) are hypertension and aging. A fundamental mechanism for hypertension- and aging-induced vascular injury is oxidative stress. We hypothesize that oxidative stress has a crucial role in ICH. To test our hypothesis, we used bacterial collagenase to produce ICH in wild-type C57BL/6 and gp91phox knockout (gp91phox KO) mice (deficient in gp91phox subunit of the superoxide-producing enzyme NADPH oxidase). All animals were studied at 20–35 weeks of age, resembling an older patient population. We found that collagenase produced less bleeding in gp91phox KO mice than wild-type mice. Total oxidative product was lower in gp91phox KO mice than in wild-type mice, both under basal conditions and after ICH. Consistent with the ICH volume, brain edema formation, neurological deficit and a high mortality rate was noted in wild-type but not in gp91phox KO mice. This ICH-induced brain injury in wild-type mice is associated with enhanced expression of the gp91phox subunit of NADPH oxidase. In conclusion, the oxidative stress resulting from activation of NADPH oxidase contributes to ICH induced by collagenase and promotes brain injury. 2005 Blackwell Publishing Journal Backfiles 1879-2005 |2005|||||||||| collagenase Liu, Jun verfasserin aut Zhou, Changman verfasserin aut Ostanin, Dmitry oth Grisham, Matthew B. oth Neil Granger, D. oth Zhang, John H. oth In Journal of neurochemistry Oxford : Wiley-Blackwell, 1956 94(2005), 5, Seite 0 Online-Ressource (DE-627)NLEJ243927584 (DE-600)2020528-4 1471-4159 nnns volume:94 year:2005 number:5 pages:0 http://dx.doi.org/10.1111/j.1471-4159.2005.03292.x text/html Verlag Deutschlandweit zugänglich Volltext GBV_USEFLAG_U ZDB-1-DJB GBV_NL_ARTICLE AR 94 2005 5 0 |
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10.1111/j.1471-4159.2005.03292.x doi (DE-627)NLEJ243113226 DE-627 ger DE-627 rakwb Tang, Jiping verfasserin aut Role of NADPH oxidase in the brain injury of intracerebral hemorrhage Oxford, UK Blackwell Science Ltd 2005 Online-Ressource nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier The major risk factors for intracerebral hemorrhage (ICH) are hypertension and aging. A fundamental mechanism for hypertension- and aging-induced vascular injury is oxidative stress. We hypothesize that oxidative stress has a crucial role in ICH. To test our hypothesis, we used bacterial collagenase to produce ICH in wild-type C57BL/6 and gp91phox knockout (gp91phox KO) mice (deficient in gp91phox subunit of the superoxide-producing enzyme NADPH oxidase). All animals were studied at 20–35 weeks of age, resembling an older patient population. We found that collagenase produced less bleeding in gp91phox KO mice than wild-type mice. Total oxidative product was lower in gp91phox KO mice than in wild-type mice, both under basal conditions and after ICH. Consistent with the ICH volume, brain edema formation, neurological deficit and a high mortality rate was noted in wild-type but not in gp91phox KO mice. This ICH-induced brain injury in wild-type mice is associated with enhanced expression of the gp91phox subunit of NADPH oxidase. In conclusion, the oxidative stress resulting from activation of NADPH oxidase contributes to ICH induced by collagenase and promotes brain injury. 2005 Blackwell Publishing Journal Backfiles 1879-2005 |2005|||||||||| collagenase Liu, Jun verfasserin aut Zhou, Changman verfasserin aut Ostanin, Dmitry oth Grisham, Matthew B. oth Neil Granger, D. oth Zhang, John H. oth In Journal of neurochemistry Oxford : Wiley-Blackwell, 1956 94(2005), 5, Seite 0 Online-Ressource (DE-627)NLEJ243927584 (DE-600)2020528-4 1471-4159 nnns volume:94 year:2005 number:5 pages:0 http://dx.doi.org/10.1111/j.1471-4159.2005.03292.x text/html Verlag Deutschlandweit zugänglich Volltext GBV_USEFLAG_U ZDB-1-DJB GBV_NL_ARTICLE AR 94 2005 5 0 |
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10.1111/j.1471-4159.2005.03292.x doi (DE-627)NLEJ243113226 DE-627 ger DE-627 rakwb Tang, Jiping verfasserin aut Role of NADPH oxidase in the brain injury of intracerebral hemorrhage Oxford, UK Blackwell Science Ltd 2005 Online-Ressource nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier The major risk factors for intracerebral hemorrhage (ICH) are hypertension and aging. A fundamental mechanism for hypertension- and aging-induced vascular injury is oxidative stress. We hypothesize that oxidative stress has a crucial role in ICH. To test our hypothesis, we used bacterial collagenase to produce ICH in wild-type C57BL/6 and gp91phox knockout (gp91phox KO) mice (deficient in gp91phox subunit of the superoxide-producing enzyme NADPH oxidase). All animals were studied at 20–35 weeks of age, resembling an older patient population. We found that collagenase produced less bleeding in gp91phox KO mice than wild-type mice. Total oxidative product was lower in gp91phox KO mice than in wild-type mice, both under basal conditions and after ICH. Consistent with the ICH volume, brain edema formation, neurological deficit and a high mortality rate was noted in wild-type but not in gp91phox KO mice. This ICH-induced brain injury in wild-type mice is associated with enhanced expression of the gp91phox subunit of NADPH oxidase. In conclusion, the oxidative stress resulting from activation of NADPH oxidase contributes to ICH induced by collagenase and promotes brain injury. 2005 Blackwell Publishing Journal Backfiles 1879-2005 |2005|||||||||| collagenase Liu, Jun verfasserin aut Zhou, Changman verfasserin aut Ostanin, Dmitry oth Grisham, Matthew B. oth Neil Granger, D. oth Zhang, John H. oth In Journal of neurochemistry Oxford : Wiley-Blackwell, 1956 94(2005), 5, Seite 0 Online-Ressource (DE-627)NLEJ243927584 (DE-600)2020528-4 1471-4159 nnns volume:94 year:2005 number:5 pages:0 http://dx.doi.org/10.1111/j.1471-4159.2005.03292.x text/html Verlag Deutschlandweit zugänglich Volltext GBV_USEFLAG_U ZDB-1-DJB GBV_NL_ARTICLE AR 94 2005 5 0 |
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Role of NADPH oxidase in the brain injury of intracerebral hemorrhage |
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The major risk factors for intracerebral hemorrhage (ICH) are hypertension and aging. A fundamental mechanism for hypertension- and aging-induced vascular injury is oxidative stress. We hypothesize that oxidative stress has a crucial role in ICH. To test our hypothesis, we used bacterial collagenase to produce ICH in wild-type C57BL/6 and gp91phox knockout (gp91phox KO) mice (deficient in gp91phox subunit of the superoxide-producing enzyme NADPH oxidase). All animals were studied at 20–35 weeks of age, resembling an older patient population. We found that collagenase produced less bleeding in gp91phox KO mice than wild-type mice. Total oxidative product was lower in gp91phox KO mice than in wild-type mice, both under basal conditions and after ICH. Consistent with the ICH volume, brain edema formation, neurological deficit and a high mortality rate was noted in wild-type but not in gp91phox KO mice. This ICH-induced brain injury in wild-type mice is associated with enhanced expression of the gp91phox subunit of NADPH oxidase. In conclusion, the oxidative stress resulting from activation of NADPH oxidase contributes to ICH induced by collagenase and promotes brain injury. |
| abstractGer |
The major risk factors for intracerebral hemorrhage (ICH) are hypertension and aging. A fundamental mechanism for hypertension- and aging-induced vascular injury is oxidative stress. We hypothesize that oxidative stress has a crucial role in ICH. To test our hypothesis, we used bacterial collagenase to produce ICH in wild-type C57BL/6 and gp91phox knockout (gp91phox KO) mice (deficient in gp91phox subunit of the superoxide-producing enzyme NADPH oxidase). All animals were studied at 20–35 weeks of age, resembling an older patient population. We found that collagenase produced less bleeding in gp91phox KO mice than wild-type mice. Total oxidative product was lower in gp91phox KO mice than in wild-type mice, both under basal conditions and after ICH. Consistent with the ICH volume, brain edema formation, neurological deficit and a high mortality rate was noted in wild-type but not in gp91phox KO mice. This ICH-induced brain injury in wild-type mice is associated with enhanced expression of the gp91phox subunit of NADPH oxidase. In conclusion, the oxidative stress resulting from activation of NADPH oxidase contributes to ICH induced by collagenase and promotes brain injury. |
| abstract_unstemmed |
The major risk factors for intracerebral hemorrhage (ICH) are hypertension and aging. A fundamental mechanism for hypertension- and aging-induced vascular injury is oxidative stress. We hypothesize that oxidative stress has a crucial role in ICH. To test our hypothesis, we used bacterial collagenase to produce ICH in wild-type C57BL/6 and gp91phox knockout (gp91phox KO) mice (deficient in gp91phox subunit of the superoxide-producing enzyme NADPH oxidase). All animals were studied at 20–35 weeks of age, resembling an older patient population. We found that collagenase produced less bleeding in gp91phox KO mice than wild-type mice. Total oxidative product was lower in gp91phox KO mice than in wild-type mice, both under basal conditions and after ICH. Consistent with the ICH volume, brain edema formation, neurological deficit and a high mortality rate was noted in wild-type but not in gp91phox KO mice. This ICH-induced brain injury in wild-type mice is associated with enhanced expression of the gp91phox subunit of NADPH oxidase. In conclusion, the oxidative stress resulting from activation of NADPH oxidase contributes to ICH induced by collagenase and promotes brain injury. |
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Role of NADPH oxidase in the brain injury of intracerebral hemorrhage |
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Liu, Jun Zhou, Changman Ostanin, Dmitry Grisham, Matthew B. Neil Granger, D. Zhang, John H. |
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