지원사업
학술연구/단체지원/교육 등 연구자 활동을 지속하도록 DBpia가 지원하고 있어요.
커뮤니티
연구자들이 자신의 연구와 전문성을 널리 알리고, 새로운 협력의 기회를 만들 수 있는 네트워킹 공간이에요.
논문 기본 정보
- 자료유형
- 학술저널
- 저자정보
- 발행연도
- 2014.12
- 수록면
- 64 - 69 (6page)
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초록· 키워드
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Objectives : Cigarette smoking had been recorded as the main cause of impaired endothelium- dependent vasodilation in smokers by reducing nitric oxide (NO), a production of endothelial nitric oxide synthase (eNOS). However, the mechanism of NO impairment via eNOS activity is unclear until now. In this study, cell passage is suggested to be a relevant factor to eNOS expression under cigarette smoking stress.
Methods : Bovine aortic endothelial cells (BAECs) were chosen as the research subject with passages ranking from 6 to 9 (6P to 9P). After exposure of cigarette smoking extract (CSE) solution, MTT assay and Western blot method were performed to check the cell viability as well as eNOS protein concentration. In these experiments, four concentrations of CSE at 0.5, 1, 2, and 4% were selected for treatment.
Results : Our results showed that cells almost died at 4% of CSE. Besides, eNOS protein mass had a linear decrease under the increase of CSE concentration. In addition, the effect of CSE on eNOS expression was dissimilar between different passages.
Conclusions : This study indicated that CSE had effect on both cell viability and eNOS expression. Besides, a reduction in protein mass was matched with the decrease of cell viability due to CSE tress. Last but not least, the response of eNOS protein to different concentration of CSE at different passages was disparate, making the hypothesis about cell passage related inhibition of eNOS caused by CSE solution.
Methods : Bovine aortic endothelial cells (BAECs) were chosen as the research subject with passages ranking from 6 to 9 (6P to 9P). After exposure of cigarette smoking extract (CSE) solution, MTT assay and Western blot method were performed to check the cell viability as well as eNOS protein concentration. In these experiments, four concentrations of CSE at 0.5, 1, 2, and 4% were selected for treatment.
Results : Our results showed that cells almost died at 4% of CSE. Besides, eNOS protein mass had a linear decrease under the increase of CSE concentration. In addition, the effect of CSE on eNOS expression was dissimilar between different passages.
Conclusions : This study indicated that CSE had effect on both cell viability and eNOS expression. Besides, a reduction in protein mass was matched with the decrease of cell viability due to CSE tress. Last but not least, the response of eNOS protein to different concentration of CSE at different passages was disparate, making the hypothesis about cell passage related inhibition of eNOS caused by CSE solution.
목차
Introduction
Materials and Methods
Results
Discussion
References
참고문헌 (16)
참고문헌 신청
Howard G / 1998 / Cigarette smoking and progression of atherosclerosis:The Atherosclerosis Risk in Communities (ARIC) Study / JAMA 279(2):119~124
Celermajer DS / 1993 / Cigarette smoking is associated with dose-related and potentially reversible impairment of endothelium-dependent dilation in healthy young adults / Circulation 88(5 Pt 1):2149~2155
Angus JA / 1989 / Endothelium-derived relaxing factor / Pharmacol Ther 41(1):303~352
Furchgott RF / 1996 / The discovery of endothelium-derived relaxing factor and its importance in the identification of nitric oxide / J Am Med Assoc 276:1186~1188
Bauer V / 2010 / Nitric oxide--the endothelium-derived relaxing factor and its role in endothelial functions / Gen Physiol Biophys 29(4):319~340
Celermajer DS / 1993 / Cigarette smoking is associated with dose-related and potentially reversible impairment of endothelium-dependent dilation in healthy young adults / Circulation 88(5 Pt 1):2149~2155
Angus JA / 1989 / Endothelium-derived relaxing factor / Pharmacol Ther 41(1):303~352
Furchgott RF / 1996 / The discovery of endothelium-derived relaxing factor and its importance in the identification of nitric oxide / J Am Med Assoc 276:1186~1188
Bauer V / 2010 / Nitric oxide--the endothelium-derived relaxing factor and its role in endothelial functions / Gen Physiol Biophys 29(4):319~340
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UCI(KEPA) : I410-ECN-0101-2016-539-002083148