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학술연구/단체지원/교육 등 연구자 활동을 지속하도록 DBpia가 지원하고 있어요.
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연구자들이 자신의 연구와 전문성을 널리 알리고, 새로운 협력의 기회를 만들 수 있는 네트워킹 공간이에요.
논문 기본 정보
- 자료유형
- 학술저널
- 저자정보
- 발행연도
- 2019.4
- 수록면
- 282 - 290 (9page)
이용수
초록· 키워드
오류제보하기
Background: Ginsenoside Rg3 (G-Rg3) is the major bioactive ingredient of Panax ginseng and has many pharmacological effects, including antiadipogenic, antiviral, and anticancer effects. However, the effect of G-Rg3 on mast cellemediated allergic inflammation has not been investigated.
Method: The antiallergic effects of G-Rg3 on allergic inflammationwere evaluated using the human and rat mast cell lines HMC-1 and RBL-2H3. Antiallergic effects of G-Rg3 were detected by measuring cyclic adenosine monophosphate (cAMP), detecting calcium influx, and using real-time reverse transcription polymerase chain reaction, enzyme-linked immunosorbent assay,Western blotting, and in vivo experiments.
Results: G-Rg3 decreased histamine release from activated mast cells by enhancing cAMP levels and calcium influx. Proinflammatory cytokine production was suppressed by G-Rg3 treatment via regulation of the mitogen-activated protein kinases/nuclear factor-kappa B and receptor-interacting protein kinase 2 (RIP2)/caspase-1 signaling pathway in mast cells. Moreover, G-Rg3 protected mice against the IgEmediated passive cutaneous anaphylaxis reaction and compound 48/80-induced anaphylactic shock.
Conclusion: G-Rg3 may serve as an alternative therapeutic agent for improving allergic inflammatory disorders.
Method: The antiallergic effects of G-Rg3 on allergic inflammationwere evaluated using the human and rat mast cell lines HMC-1 and RBL-2H3. Antiallergic effects of G-Rg3 were detected by measuring cyclic adenosine monophosphate (cAMP), detecting calcium influx, and using real-time reverse transcription polymerase chain reaction, enzyme-linked immunosorbent assay,Western blotting, and in vivo experiments.
Results: G-Rg3 decreased histamine release from activated mast cells by enhancing cAMP levels and calcium influx. Proinflammatory cytokine production was suppressed by G-Rg3 treatment via regulation of the mitogen-activated protein kinases/nuclear factor-kappa B and receptor-interacting protein kinase 2 (RIP2)/caspase-1 signaling pathway in mast cells. Moreover, G-Rg3 protected mice against the IgEmediated passive cutaneous anaphylaxis reaction and compound 48/80-induced anaphylactic shock.
Conclusion: G-Rg3 may serve as an alternative therapeutic agent for improving allergic inflammatory disorders.
목차
ABSTRACT
1. Introduction
2. Materials and methods
3. Results
4. Discussion
References
참고문헌 (40)
참고문헌 신청
Galli SJ / 2005 / Mast cells as"tunable"effector and immunoregulatory cells : recent advances / Annu Rev Immunol 23:749~786
Galli SJ / 2010 / Mast cells in allergy and infection : versatile effector and regulatory cells in innate and adaptive immunity / Eur J Immunol 40:1843~1851
Johnson GL / 2002 / Mitogen-activated protein kinase pathways mediated by ERK, JNK, and p38 protein kinases / Science 298:1911~1912
May MJ / 1998 / Signal transduction through NF-kappa B / Immunol Today 19:80~88
Barnes PJ / 1997 / Nuclear factor-kappaB : a pivotal transcription factor in chronic inflammatory diseases / N Engl J Med 336:1066~1071
Galli SJ / 2010 / Mast cells in allergy and infection : versatile effector and regulatory cells in innate and adaptive immunity / Eur J Immunol 40:1843~1851
Johnson GL / 2002 / Mitogen-activated protein kinase pathways mediated by ERK, JNK, and p38 protein kinases / Science 298:1911~1912
May MJ / 1998 / Signal transduction through NF-kappa B / Immunol Today 19:80~88
Barnes PJ / 1997 / Nuclear factor-kappaB : a pivotal transcription factor in chronic inflammatory diseases / N Engl J Med 336:1066~1071
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