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Urotensin II 수용체 길항제에 의한 혈관증식 억제 효능 및 기전
| DC Field | Value | Language |
|---|---|---|
| dc.contributor.advisor | 정이숙 | - |
| dc.contributor.author | 이동길 | - |
| dc.date.accessioned | 2018-11-08T08:21:38Z | - |
| dc.date.available | 2018-11-08T08:21:38Z | - |
| dc.date.issued | 2015-02 | - |
| dc.identifier.other | 18896 | - |
| dc.identifier.uri | https://dspace.ajou.ac.kr/handle/2018.oak/13064 | - |
| dc.description | 학위논문(석사)--아주대학교 일반대학원 :약학,2015. 2 | - |
| dc.description.tableofcontents | Abstract i TABLE OF CONTENTS iii LIST OF FIGURES v ABBREVIATION vi Ⅰ. INTRODUCTION 1 A. Atherosclerosis 1 B. Urotensin II 1 C. Antagonists 2 D. Aims 2 Ⅱ. MATERIALS AND METHODS 3 A. Chemicals and Reagents 3 B. Cell culture 3 C. 5-bromo-2'-deoxyuridine (BrdU) incorporation 4 D. Western blotting 4 E. Measurements of reactive oxygen species (ROS) release 5 F. Mouse carotid ligation model 5 G. Hematoxylin and eosin staining 6 H. Statistical analysis 7 Ⅲ. RESULTS 8 A. Effect of KR-36676 and KR-36996 on SMC proliferation. 8 B. Inhibitory of inhibitors on UII-induced proliferation in hAoSMCs. 10 C. UII-induced ROS generation in HASMC on time course. 11 D. Effect of KR-36676 on UII-induced ROS generation in hAoSMCs. 13 E. Effect of KR-36996 on UII-induced ROS generation in hAoSMCs. 16 F. Effect of KR-36676 on UII-induced ERK activation in hAoSMCs. 18 G. Effect of KR-36996 on UII-induced ERK activation in hAoSMCs. 20 H. Effect of KR-36676 on carotid ligation-induced intimal thickening. 22 I. Effect of KR-36996 on carotid ligation-induced intimal thickening. 24 Ⅳ. DISCUSSION 26 Ⅴ. CONCLUSION 30 REFERENCES 31 국문요약 34 | - |
| dc.language.iso | eng | - |
| dc.publisher | The Graduate School, Ajou University | - |
| dc.rights | 아주대학교 논문은 저작권에 의해 보호받습니다. | - |
| dc.title | Urotensin II 수용체 길항제에 의한 혈관증식 억제 효능 및 기전 | - |
| dc.title.alternative | Lee Dong-Gil | - |
| dc.type | Thesis | - |
| dc.contributor.affiliation | 아주대학교 일반대학원 | - |
| dc.contributor.alternativeName | Lee Dong-Gil | - |
| dc.contributor.department | 일반대학원 약학 | - |
| dc.date.awarded | 2015. 2 | - |
| dc.description.degree | Master | - |
| dc.identifier.localId | 695443 | - |
| dc.identifier.url | http://dcoll.ajou.ac.kr:9080/dcollection/jsp/common/DcLoOrgPer.jsp?sItemId=000000018896 | - |
| dc.subject.keyword | Urotensin II | - |
| dc.subject.keyword | Urotensin II receptor | - |
| dc.subject.keyword | Urotensin II receptor antagonists | - |
| dc.subject.keyword | Atherosclerosis | - |
| dc.subject.keyword | ERK | - |
| dc.subject.keyword | ROS | - |
| dc.subject.keyword | Proliferation | - |
| dc.subject.keyword | ligation. | - |
| dc.description.alternativeAbstract | Urotensin-II (UII) is a vasoactive peptide that promotes vascular smooth muscle cell proliferation and is involved in the pathogenesis of atherosclerosis, restenosis and vascular remodeling. In this study, effects of KR-36676 and KR-36996, a novel selective urotensin receptor (UT) antagonist, on smooth muscle cell proliferation was examined. UII-induced proliferation of human aortic smooth muscle cells (hAoSMCs), was found to be significantly inhibited by KR-36676 and KR-36996 (1, 10, and 100 nM) in dose-dependent manner. UII-induced proliferation of hAoSMCs cells was also inhibited by U0126, an ERK1/2 inhibitor, but not by SP600125 and SB202190, inhibitors of JNK and p38 MAPK, respectively. UII increased the phosphorylation of ERK1/2, but this increase was significantly inhibited by KR-36676 and KR-36996. In addition, the UII-induced proliferation was also inhibited by trolox, a scavenger of reactive oxygen species (ROS), while the UII-induced ROS was also decreased in response to KR-36676 and KR-36996 treatment. Moreover, in a carotid artery ligation mouse model, intimal thickening was dramatically suppressed by oral treatment with KR-36676 and KR-36996 (30 mg/kg). Taken together, KR-36676 and KR-36996 attenuated UII-induced proliferation of hAoSMCs cells, at least partially, through blocking ERK1/2 activation and ROS generation. | - |
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