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
- 저널정보
- 대한외과학회 Annals of Surgical Treatment and Research Annals of Surgical Treatment and Research Vol.97 No.4
- 발행연도
- 2019.10
- 수록면
- 159 - 167 (9page)
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초록· 키워드
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Purpose: Almost all liver diseases are known to be accompanied by increased levels of reactive oxygen species (ROS), regardless of the cause of the liver disorder. However, little is known about the role of hypoxic conditioned media (HCM) in the view of pro-oxidative/antioxidative balance.
Methods: Normoxic conditioned media (NCM) and HCM were obtained after culturing adipose-derived stem cells in 20% O₂ or 1% O₂ for 24 hours, respectively. Their effects on the expression of various markers reflecting pro-oxidative/antioxidative balance were investigated in both in vitro (thioacetamide-treated AML12 cells) and in vivo (partially hepatectomized mice) models of liver injury, respectively.
Results: HCM treatment induced the higher expression of antioxidant enzymes, such as superoxide dismutase, glutathione peroxidase, and catalase than did NCM in the in vitro model of liver injury. We also found that HCM increased the expression of nuclear factor erythroid 2–related factor (NRF2). The in vivo models of liver injury consistently validated the phenomenon of upregulated expression of antioxidant enzymes by HCM.
Conclusion: We thus could conclude that HCM provides protection against ROS-related toxicity by increasing the expression of antioxidant enzymes, in part by releasing NRF2 in the injured liver.
Methods: Normoxic conditioned media (NCM) and HCM were obtained after culturing adipose-derived stem cells in 20% O₂ or 1% O₂ for 24 hours, respectively. Their effects on the expression of various markers reflecting pro-oxidative/antioxidative balance were investigated in both in vitro (thioacetamide-treated AML12 cells) and in vivo (partially hepatectomized mice) models of liver injury, respectively.
Results: HCM treatment induced the higher expression of antioxidant enzymes, such as superoxide dismutase, glutathione peroxidase, and catalase than did NCM in the in vitro model of liver injury. We also found that HCM increased the expression of nuclear factor erythroid 2–related factor (NRF2). The in vivo models of liver injury consistently validated the phenomenon of upregulated expression of antioxidant enzymes by HCM.
Conclusion: We thus could conclude that HCM provides protection against ROS-related toxicity by increasing the expression of antioxidant enzymes, in part by releasing NRF2 in the injured liver.
목차
INTRODUCTION
METHODS
RESULTS
REFERENCES
참고문헌 (28)
참고문헌 신청
Baglio SR / 2012 / Mesenchymal stem cell secreted vesicles provide novel opportunities in(stem)cell-free therapy / Front Physiol 3:359
Fink T / 2004 / Induction of adipocyte-like phenotype in human mesenchymal stem cells by hypoxia / Stem Cells 22:1346~1355
Lee SC / 2016 / Hypoxic conditioned medium from human adipose-derived stem cells promotes mouse liver regeneration through JAK/STAT3 signaling / Stem Cells Transl Med 5:816~825
Lee SC / 2017 / Determination of optimized oxygen partial pressure to maximize the liver regenerative potential of the secretome obtained from adipose-derived stem cells / Stem Cell Res Ther 8:181
Liu L / 2013 / Hypoxia preconditioned human adipose derived mesenchymal stem cells enhance angiogenic potential via secretion of increased VEGF and bFGF / Cell Biol Int 37:551~560
Fink T / 2004 / Induction of adipocyte-like phenotype in human mesenchymal stem cells by hypoxia / Stem Cells 22:1346~1355
Lee SC / 2016 / Hypoxic conditioned medium from human adipose-derived stem cells promotes mouse liver regeneration through JAK/STAT3 signaling / Stem Cells Transl Med 5:816~825
Lee SC / 2017 / Determination of optimized oxygen partial pressure to maximize the liver regenerative potential of the secretome obtained from adipose-derived stem cells / Stem Cell Res Ther 8:181
Liu L / 2013 / Hypoxia preconditioned human adipose derived mesenchymal stem cells enhance angiogenic potential via secretion of increased VEGF and bFGF / Cell Biol Int 37:551~560
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