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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.
초록· 키워드
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Objective : This study aimed to evaluate the protective effects of Gamipalmi-hwan (GPH) on elastase-induced lung cell injury.
Materials and Methods : As an in vitro model of emphysema, the current study was performed to investigate potential activity of GPH in regulating injury responses of A549 human type II cell line mediated by elastase treatment.
Results : GPH treatment increased the number of A549 cells which was reduced by elastase digestion. Elastin protein level, which was reduced by elastase treatment, was increased by GPH treatment. Labeling intensity with caspase 3 protein in elastase-treated cells was reduced by GPH treatment. Both Erk1/2 and Cdc2 protein levels, which were decreased by elastase treatment, were increased to a level similar to that of the normal cells. mRNA levels encoding IL-1β and TNF-α were increased by elastase and then down-regulated by GPH.
Conclusion : The present data suggest that A549 cells are subjected to inflammatory damage by elastase and can be recovered by GPH treatment. Further studies examining the protective activity of GPH in elastase-treated lung tissue would be useful for therapeutic strategies of emphysema treatment.
Materials and Methods : As an in vitro model of emphysema, the current study was performed to investigate potential activity of GPH in regulating injury responses of A549 human type II cell line mediated by elastase treatment.
Results : GPH treatment increased the number of A549 cells which was reduced by elastase digestion. Elastin protein level, which was reduced by elastase treatment, was increased by GPH treatment. Labeling intensity with caspase 3 protein in elastase-treated cells was reduced by GPH treatment. Both Erk1/2 and Cdc2 protein levels, which were decreased by elastase treatment, were increased to a level similar to that of the normal cells. mRNA levels encoding IL-1β and TNF-α were increased by elastase and then down-regulated by GPH.
Conclusion : The present data suggest that A549 cells are subjected to inflammatory damage by elastase and can be recovered by GPH treatment. Further studies examining the protective activity of GPH in elastase-treated lung tissue would be useful for therapeutic strategies of emphysema treatment.
목차
서론
재료와 방법
결과
고찰
결론
참고문헌
참고문헌 (32)
참고문헌 신청
1. [학술지(정기간행물)] - Doree M / 2002 / From Cdc2 to Cdk1: when did the cell cycle kinase join its cyclin partner? / J Cell Sci. 115 (12) : 2461 ~ 2464
2. [학술지(정기간행물)] - Nebreda AR / 2006 / CDK activation by non-cyclin proteins / Curr Opin Cell Biol 18 (2) : 192 ~ 198
3. [학술지(정기간행물)] - Goga A / 2007 / Inhibition of CDK1 as a potential therapy for tumors over-expressing MYC / Nat Med 13 (7) : 820 ~ 827
4. [학술지(정기간행물)] - Sapey E / 2009 / Imbalances between interleukin-1 and tumor necrosis factor agonists and antagonists in stable COPD / J Clin Immunol 29 (4) : 508 ~ 516
5. [학술지(정기간행물)] - Suki B / 2008 / Extracellular matrix mechanics in lung parenchymal diseases / Respir Physiol Neurobiol 163 (1) : 33 ~ 43
2. [학술지(정기간행물)] - Nebreda AR / 2006 / CDK activation by non-cyclin proteins / Curr Opin Cell Biol 18 (2) : 192 ~ 198
3. [학술지(정기간행물)] - Goga A / 2007 / Inhibition of CDK1 as a potential therapy for tumors over-expressing MYC / Nat Med 13 (7) : 820 ~ 827
4. [학술지(정기간행물)] - Sapey E / 2009 / Imbalances between interleukin-1 and tumor necrosis factor agonists and antagonists in stable COPD / J Clin Immunol 29 (4) : 508 ~ 516
5. [학술지(정기간행물)] - Suki B / 2008 / Extracellular matrix mechanics in lung parenchymal diseases / Respir Physiol Neurobiol 163 (1) : 33 ~ 43
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UCI(KEPA) : I410-ECN-0101-2014-519-000285475