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담배 니코틴에 의한 사람 태아 성상세포에서 종양괴사인자(TNF-α)의 발현 억제작용
손일홍,이성익,양현덕,한선정,석승한,이재규,김재현,박주영,문형인,이성수,Son, Il-Hong,Lee, Sung-Ik,Yang, Hyun-Duk,Han, Sun-Jung,Suk, Seung-Han,Lee, Jai-Kyoo,Kim, Jae-Hyun,Park, Joo-Young,Moon, Hyung-In,Lee, Sung-Soo 대한화학회 2007 대한화학회지 Vol.51 No.3
니코틴은 사람 대식세포에서 interleukin 2 (IL-2)와 종양괴사인자 (tumor necrosis factor-alpha; TNF-α) 가 생성되는 것을 억제하는데, 이러한 억제작용은 cytokine 유전자 발현 중 전사단계에서 전사인자의 활성을 억제함으로써 일어난다. 이러한 니코틴의 면역반응 억제작용은 아프타성궤양 및 궤양성대장염, 알레르기성폐 포염, 건초열 등에서도 보고되고 있다. 만일 중추신경계에서도 위와 같은 니코틴의 면역억제 작용이 일어난 다면 다발성경화증과 같은 면역반응 매개질환의 치료에 새로운 전기가 마련될 수 있을 것이다. 본 연구에서 는 중추신경계의 여러 면역반응 매개질환의 병태생리에 대한 이해를 넓히고자, 이미 알려진 니코틴의 cytokine 생성억제가 사람 중추신경계의 성상세포에서도 일어남을 확인하고 그 억제기전을 밝히고자 하였다. 이를 위 하여 사람 태아 성상세포에 다양한 농도의 니코틴과 IL-1β를 처리한 다음 TNF-α mRNA의 발현 정도와 NF- κB의 활성을 비교, 분석하여 다음과 같은 결과를 얻었다. 1. 사람 태아 성상세포를 0.1-20 μg/ml의 니코틴으로 처리해 본 결과 10 μg/ml 이상의 농도에서 세포독성능이 나타나기 시작하였다. 2. 사람 태아 성상세포에 IL- 1β를 처리하면 2시간만에 TNF-α mRNA가 최대로 발현되었으며 그 이후로는 점진적으로 감소하였다. 3. 사 람 태아 성상세포를 1 및 0.1 μg/ml의 니코틴으로 전처리한 후 IL-1β로 자극한 군에서는 IL-1β 단독 처리군에 비해 TNF-α mRNA의 발현이 감소하는 양상을 보였다. 1 μg/ml의 니코틴을 처리한 경우에는 8시간 이후부터 TNF-α mRNA의 발현이 현저하게 감소하여 12시간에 최대로 감소하였다. 또한 0.1 μg/ml의 니코틴을 처리한 군에서는 24시간에 가장 현저하게 감소하였다. 4. 성상세포에 IL-1β로 처리한 군에서는 강력한 NF-κB의 활성 을 확인할 수 있었으며, 니코틴을 전처리하고 IL-1β 자극한 군에서는 NF-B의 활성이 감소하였다. 결론적으로 일정농도 이상의 니코틴은 세포독성효과를 나타내나 적정한 농도와 시간 경과후 니코틴은 사람 태아 성상세포에서 IL-1β에 의해 유도되는 TNF-α의 발현 감소를 유도하며, 이는 NF-κB의 활성을 감소시킴으로써 나타난다고 생각된다. The Tumor necrosis factor-α, (TNF-α), is involved in the pathogenesis of multiple sclerosis and contributes to the degeneration of oligodendrocytes as well as neurons. Nicotine has been found to have immunosuppressive and inflammation-suppressing effects. Astrocytes, the major glial cells in the CNS, are capable of producing TNF-α at both the mRNA and protein levels in response to interleukin-1 (IL-1) or TNF-α. Nicotine has been shown to influence glial cell functions. To order to explore the role of astrocytes in the production of TNF-α, astrocytes were pretreated with nicotine and are stimulated with IL-1β to determine their effects on TNF-α production. The results are as follows. Cytotoxic effects of nicotine on human fetal astrocytes were noted above 10 μg/ml of nicotine. The effect of IL-1β on TNF-α mRNA expression in primary cultured human fetal astrocytes was maximal at 2 h after IL- 1β(100 pg/ml) treatment. Human fetal astrocytes were pretreated with 0.1, 1, and 10 μg/ml of nicotine and then stimulated with IL-1β (100 pg/ml) for 2 h. The inhibitory effect of nicotine on expressions of TNF-α mRNA in human fetal astrocytes with pretreated 0.1 μg/ml of nicotine is first noted at 8 hr, and the inhibitory effect is maximal at 12 h. The inhibitory effect at 1 μg/ml of nicotine is inhibited maximal at 24 h. Nicotine at 0.1, 1 and 10 μg/ml concentrations significantly inhibits IL-1β-induced NF-κB activation. Collectively, this study indicates that nicotine might inhibit the expression of TNF-α in activated human fetal astrocytes.
H2O2로 유도된 산화적 스트레스에 대한 장원환가감방(壯元丸加減方)의 PC 12 cell 에서의 항산화 효과
박용훈 ( Yong Hoon Park ),손일홍 ( Il Hong Son ),이상원 ( Sang Won Lee ),임정현 ( Jung Hyun Lim ),김태헌 ( Tae Heon Kim ),류영수 ( Yeoung Su Lyu ),강형원 ( Hyung Won Kang ) 대한한방신경정신과학회 2009 동의신경정신과학회지 Vol.20 No.2
Objectives: Antioxidant effects of Gagam-Jangwonhwan(LMK01 and 02) water extract against H2O2-induced oxidative damage and cell death were investigated in rat pheochromocytoma line PC 12. Methods: The cells were treated with LMK01 and 02 water extract and H2O2, oxidative damage-inducing materials for 24 h. The cellular viability was assessed by WST-1 assay, oxidative damages of the cells by 8-OHdG quantitation, apoptosis by Hoechst 33342 staining assay and activity of antioxidant enzymes by catalase and glutathione peroxidase assay. Results: 1. LMK01 and LMK02 water extracts improved significantly cell viability in H2O2-treated groups than H2O2-alone treated cells 2. LMK02 suppressed significantly oxidative damage in H2O2-treated groups than H2O2-alone treated cells but LMK01 didn`t. Meanwhile, difference of oxidative damages in conditions treated with LMK01 or LMK02 was not significant, 3. The H2O2 induced-apoptosis in PC 12 cell lines was inhibited effectively by LMK01 and LMK02, and especially the features of apoptosis were obviously reduced in LMK02-treated cells. 4. LMK01 and LMK02 increased significantly activities of both catalase and glutathione peroxidase than those of H2O2-alone treated group and moreover, LMK02 showed significantly higher activities than those of LMK01. Conclusions: As shown, LMK01 and LMK02 suppressed H2O2-induced oxidative damage and cell death in PC 12 cell effectively. And they increased activity of major antioxidant enzymes in PC 12 cell line. Therefore, this study suggests the possibility of clinical usage over oxidative stress-induced neurodegenerative disease such as Alzheimer`s disease.
Wallenberg`s syndrome 치험(治驗) 1례(例)를 통해 본 동(東).서협진(西協診) 유형(類型) 연구(硏究)(1)
장현호 ( Hyun Ho Jang ),양현덕 ( Hyun Duk Yang ),민양기 ( Yang Ki Min ),손일홍 ( Il Hong Son ),석승한 ( Seung Han Suk ),민상준 ( Sang Joon Min ),류영수 ( Yeoung Su Lyu ),이건목 ( Geon Mok Lee ),강형원 ( Hyung Won Kang ) 대한한방신경정신과학회 2001 동의신경정신과학회지 Vol.12 No.1
손일홍,양현웅,이재규,이강창 대한동의병리학회 2003 동의생리병리학회지 Vol.17 No.3
It has been demonstrated that oxidative stress of reactive oxygen species(ROS) may be a causative factor in the pathogenesis of bony disorder. The purpose of this study was to evaluate the oxidative stress of glucose oxidase(GO) in the cultured mouse osteoblasts and the protective effect of Alli Macrostemi Bulbus(AMB) on ROS-induced osteotoxicity. Toxic effect of GO and protective effect of AMB were carried out by colorimetric assay. 20mU/ml GO decreased cell viability dose-dependently, and AMB increased cell viability against GO-induced cytotoxicity in these cultures. From above the results, GO has toxic effect, and AMB is very effective on GO-induced osteotoxicity in cultured osteoblasts of neonatal mouse.