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Sevoflurane post-conditioning increases nuclear factor erythroid 2-related factor and hemoxygenase-1 expression via protein kinase C pathway in a rat model of transient global cerebral ischemia : 백서의 일과성 전뇌허혈 모델에서 sevoflurane 후처치 후 PKC 경로를 통한 Nrf2와 HO-1의 발현 증가
DC Field | Value | Language |
---|---|---|
dc.contributor.advisor | 박희평 | - |
dc.contributor.author | 이한나 | - |
dc.date.accessioned | 2017-07-14T01:29:51Z | - |
dc.date.available | 2017-07-14T01:29:51Z | - |
dc.date.issued | 2015-02 | - |
dc.identifier.other | 000000024843 | - |
dc.identifier.uri | https://hdl.handle.net/10371/122027 | - |
dc.description | 학위논문 (박사)-- 서울대학교 대학원 : 의학과, 2015. 2. 박희평. | - |
dc.description.abstract | Introduction: The antioxidant mechanism of sevoflurane postconditioning-induced neuroprotection remains unclear. We determined whether sevoflurane postconditioning induces nuclear factor erythroid 2-related factor (Nrf2, a master transcription factor regulating antioxidant defense genes) and heme oxygenase-1 (HO-1, an antioxidant enzyme) expression, and whether protein kinase C (PKC) is involved in Nrf2 activation in a rat model of transient global cerebral ischemia/reperfusion (IR) injury.
Methods: 86 rats were assigned to five groups: sham (n=6), control (n=20), sevoflurane postconditioning (two cycles with 2 vol% sevoflurane inhalation for 10 min, n=20), chelerythrine (a PKC inhibitor | - |
dc.description.abstract | 5 mg kg-1 intravenous administration, n=20), and sevoflurane postconditioning plus chelerythrine (n=20). Each group was further divided into two subgroups, based on the day of sacrifice (1 or 7 days after ischemia), of 10 rats each, except sham group (n=3). The levels of nuclear Nrf2 and cytoplasmic HO-1 were assessed.
Results: On day 1 post-ischemia, but not day 7, Nrf2 and HO-1 expression was significantly higher in the sevoflurane postconditioning group than in the control group. Chelerythrine administration reduced Nrf2 and HO-1 expression induced by sevoflurane postconditioning. Conclusions: Sevoflurane postconditioning increased Nrf2/HO-1 expression via PKC signaling in the early phase after transient global cerebral IR injury, suggesting that activation of antioxidant enzymes may be responsible for sevoflurane postconditioning-induced neuroprotection in the early phase after cerebral IR injury. | - |
dc.description.tableofcontents | Abstract i
Contents iii List of Tables and Figures ⅳ Introduction 2 Material and Methods 4 Results 12 Discussion 24 References 31 Korean Abstract 40 | - |
dc.format | application/pdf | - |
dc.format.extent | 738595 bytes | - |
dc.format.medium | application/pdf | - |
dc.language.iso | en | - |
dc.publisher | 서울대학교 대학원 | - |
dc.subject | Anesthetics | - |
dc.subject | inhalation | - |
dc.subject.ddc | 610 | - |
dc.title | Sevoflurane post-conditioning increases nuclear factor erythroid 2-related factor and hemoxygenase-1 expression via protein kinase C pathway in a rat model of transient global cerebral ischemia | - |
dc.title.alternative | 백서의 일과성 전뇌허혈 모델에서 sevoflurane 후처치 후 PKC 경로를 통한 Nrf2와 HO-1의 발현 증가 | - |
dc.type | Thesis | - |
dc.contributor.AlternativeAuthor | Hannh Lee | - |
dc.description.degree | Doctor | - |
dc.citation.pages | 41 | - |
dc.contributor.affiliation | 의과대학 의학과 | - |
dc.date.awarded | 2015-02 | - |
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