VEGF Antagonism Attenuates Cerebral Ischemia/Reperfusion-Induced Injury via Inhibiting Endoplasmic Reticulum Stress-Mediated Apoptosis
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- Feng Shu-Qing
- Department of Ultrasound, The First People’s Hospital of Yunnan Province Department of Ultrasound, The Affiliated Hospital of Kunming University of Science and Technology
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- Zong Shao-Yun
- Department of Ultrasound, The First People’s Hospital of Yunnan Province Department of Ultrasound, The Affiliated Hospital of Kunming University of Science and Technology
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- Liu Jia-Xin
- Medical School of Kunming University of Science and Technology
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- Chen Yang
- Department of Ultrasound, The First People’s Hospital of Yunnan Province Department of Ultrasound, The Affiliated Hospital of Kunming University of Science and Technology
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- Xu Rong
- Department of Ultrasound, The First People’s Hospital of Yunnan Province Department of Ultrasound, The Affiliated Hospital of Kunming University of Science and Technology
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- Yin Xin
- Department of Ultrasound, The First People’s Hospital of Yunnan Province Department of Ultrasound, The Affiliated Hospital of Kunming University of Science and Technology
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- Zhao Rong
- Yunnan province Hospital of Traditional Chinese Medical
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- Li Ying
- Department of Rehabilitation, The First People’s Hospital of Yunnan Province Department of Rehabilitation, The Affiliated Hospital of Kunming University of Science and Technology
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- Luo Ting-Ting
- Department of Ultrasound, The First People’s Hospital of Yunnan Province Department of Ultrasound, The Affiliated Hospital of Kunming University of Science and Technology
書誌事項
- タイトル別名
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- VEGF Antagonism Attenuates Cerebral Ischemia/Reperfusion-Induced Injury <i>via</i> Inhibiting Endoplasmic Reticulum Stress-Mediated Apoptosis
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<p>Endoplasmic reticulum (ER) stress-mediated apoptosis pathway is considered to play a vital role in mediating stroke and other cerebrovascular diseases. Previous studies have showed that vascular endothelial growth factor (VEGF) antagonism reduced cerebral ischemic–reperfusion (CI/R) damage, but whether attenuation of ER stress-induced apoptosis is contributing to its mechanisms remains elusive. Our study aimed to investigate the protective effect of VEGF antagonism on CI/R-induced injury. First, oxygen–glucose deprivation and re-oxygenation (OGD/R) BEND3 cell model was constructed to estimate small interfering RNA (siRNA)-VEGF on damage of endothelial cells. Next, in animal model, CI/R mice were induced by middle cerebral artery occlusion (MCAO) for 2 h followed by 24 h reperfusion to investigate cerebral tissue damage. For treatment group, mice received 100 µg/kg anti-VEGF antibodies at 30 min before MCAO, followed by 24 h reperfusion. Our findings demonstrated that pre-administration of siRNA-VEGF before OGD/R changed the biological characteristics of BEND3 cells, reversed the levels of X-box binding protein-1 (XBP-1) and glucose-regulated protein 78 (GRP78), showing siRNA-VEGF attenuated, at least in part, the oxidative damage in OGD/R cell by down-regulating ER stress. In mice experiment, pre-administration of anti-VEGF antibody reduced the brain infarct volume and edema extent and improved neurological scores outcome of CI/R injury mice. Pathological and terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate nick-end labeling (TUNEL) staining results also confirmed this protective effect. The expressions of VEGF, CATT/EBP homologous protein (CHOP), inositol requiring enzyme 1α (IRE-1α), and cleaved-caspase12 and c-jun N-terminal kinase (JNK) phosphorylation were also prominently decreased. These results suggested that inhibition of endogenous VEGF attenuates CI/R-induced injury via inhibiting ER stress-mediated apoptosis.</p>
収録刊行物
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- Biological & Pharmaceutical Bulletin
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Biological & Pharmaceutical Bulletin 42 (5), 692-702, 2019-05-01
公益社団法人 日本薬学会
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詳細情報 詳細情報について
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- CRID
- 1390001288135480320
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- NII論文ID
- 130007641423
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- NII書誌ID
- AA10885497
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- ISSN
- 13475215
- 09186158
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- NDL書誌ID
- 029657669
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- PubMed
- 30828041
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- 本文言語コード
- en
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- データソース種別
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- JaLC
- NDL
- Crossref
- PubMed
- CiNii Articles
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- 使用不可