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.

인간 재조합 인터루긴-32 면역조절작용에 대한 유세포 분석

이광수,김영관,채정일,심정현,김은미,강형식,김수현,윤도영,명평근 충남대학교 생물공학연구소 2006 생물공학연구지 Vol.12 No.-

Xenotransplantation of porcine organs has the potential to overcome the severe shortage of human tissues and organ available for human transplantation. however, it remains various hurdles for clinical xenotransplantation. In pig and mouse xenotransplantation, porcine xenograft evoke a strong cellular rejection response in immunocompetent host and grafts are destroyed within a week. This cellular immune response could involved both T cells and NK cells. A number of groups have shown that human NK cells can recognize and damage porcine endothelial cells. In addition, human T cells can respond to porcine endothelial cells through both direct and indirect mechanisms. Cellular rejection of porcine tissues requires T cells, particularly CD4^(+) cells. A new cytokine recombinant human interleukin-32α,β(IL-32α,β) has a role innate and acquired immune system. In order to investigate the role of recombinant mouse IL-18 and recombinant human IL-32α,β in xenograft rejection, we transplanted the PK(15) cells to C57BL/6 mice with or without intraperitoneal injection of recombinant mouse IL-18 or recombinant human IL-32 α,β. It was analyzed the population of NK cell, T cell and B cell in the C57BL/6 mice transplanted with PK(15) cells and recombinant mouse IL-18 or recombinant human IL-32α,β by flow cytometry analysis. As a result, lymph node and thymus of PK15/IL18, PK15/IL32α and PK15/IL32β injected group were increased to T cell activation population than normal injected groups. CD8^(+) T cells were decreased in lymph node of PK15/IL18, PK15/IL32α and PK15/IL32β injected groups. CD4^(+) T cells were increased in lymph node cell of PK15/IL32α and PK15/IL32β injected group and also, B cell population were increased in lymph node cell and spleen of PK15/IL18, PK15/IL32α and PK15/IL32β injected group. Therefore, we suggest that recombinant mouse IL-18 and recombinant human IL-32α,β suppress xenograft rejection in cellular xenotransplantation.

Decreased Pattern-Recognition Receptor-Mediated Cytokine mRNA Expression in Obese Children With Otitis Media With Effusion

Kim, Youn Jung,Cha, Sung Ho,Lee, Ho Yun,Lee, Sun Kyu,Chung, Hee Yong,Yeo, Joon Hyung,Kim, Young Il,Yeo, Seung Geun Korean Society of Otorhinolaryngology-Head and Nec 2014 Clinical and Experimental Otorhinolaryngology Vol.7 No.1

<P><B>Objectives</B></P><P>To assess innate and humoral immune responses in middle ear effusion of obese pediatric patients with otitis media with effusion (OME).</P><P><B>Methods</B></P><P>We evaluated 219 children with OME, of whom 21 were obese and 198 were non-obese. We compared the expression in middle ear effusion of mRNAs encoding toll-like receptors (TLR) 2, 4, 5, and 9; nucleotide-binding oligomerization domains (NOD) 1 and 2; retinoic acid-inducible gene (RIG)-I; interleukins (IL)-6, -10, and -12; interferon (IFN)-γ; and tumor necrosis factor (TNF)-α mRNAs. We also compared the expression of immunoglobulins IgG, IgA, and IgM and the bacterial detection rate in the two groups.</P><P><B>Results</B></P><P>TLR2-mediated expression of IL-6 mRNA, TLR4-mediated expression of IL-6 and IL-10 mRNA, TLR5-mediated expression of IL-6, IL-10, and TNF-α mRNA, TLR9-mediated expression of IL-6 mRNA, and NOD2-mediated expression of IL-6, IL-12, and TNF-α mRNA were significantly lower in obese than in non-obese children (<I>P</I><0.05). However, concentrations of IgG, IgA, and IgM in middle ear effusion were lower in obese than in non-obese children, but none of these differences was significant (<I>P</I>>0.05).</P><P><B>Conclusion</B></P><P>Mean body mass index was higher and pattern-recognition receptor-mediated cytokine mRNA expression was lower in obese than in non-obese children with OME.</P>

N-Acetyl-L-Cysteine에 의한 생쥐 골수유래 가지세포의 기능적 활성화 저해

정영주(Young-joo Jeong),맹형건(Hyung Gun Maeng),김민규(Min Kyu Kim),강재승(Jae Seung Kang),이왕재(Wang Jae Lee),황영일(Young-il Hwang) 대한해부학회 2008 Anatomy & Cell Biology Vol.41 No.2

N-acetyl-L-cysteine (NAC)은 thiol기를 포함하는 화합물로서, glutathione (GSH)의 전구체로 작용하여 포유류 세포 내에서 항산화제로 작용한다. 또한 항염기능이 있으며 호산구나 B세포, 가지세포 (dendritic cell, DC)와 같은 면역세포 들에 여러 가지 영향을 미치는 것으로 알려져 있다. 특히 가지세포에 작용하여 활성화를 억제하거나 가지세포에 의한 Th2 반응 유도에 관여한다고 알려져 있다. 그러나 이들 연구는 세부적인 사항에 있어서 그 결과가 서로 상치하는바가 많으며, 또한 조절T세포의 관점에서는 연구된 바가 없다. 따라서 본 연구에서는 NAC 처리가 가지세포 활성화에 미치는 영향을 재확인하였고, NAC 처리된 가지세포의 T세포 활성 능력 저하, 또는 Th2 반응 유도 여부를 알아보았다. 활성화 시 가지세포에서 증가하는 활성산소기 (reactive oxygen species)는 NAC 처리로 낮아져서, NAC이 가지세포에 항산화작용을 나타냄을 확인하였다. NAC 처리로 가지세포에서 보조자극인자인 CD40과 CD86의 발현이 저해되었으며, 활성화 시 정상적으로 낮아지는 포식기능은 처리된 NAC의 농도에 비례하게 보존되었다. 활성화 시 분비되는 IL-6, IL-10, IL-12는 모두 감소하였다. 이러한 NAC-DC와 함께 배양한 T세포의 증식이나 Th1 cytokine인 IFN-γ, Th2 cytokine인 IL-5의 분비가 모두 저하되어 Th1/Th2의 편중 없이 가지세포의 T세포 자극능력이 전반적으로 감소하였음을 나타내었다. 또한 T세포 배양액에서 IL-10과 TGF-β의 농도 역시 NAC-DC로 자극된 경우에 현저히 줄어서, NAC-DC에 의한 T세포 증식 감소 등은 조절T세포 유도에 의한 것이 아니라 T세포 무반응이 유도된 때문임을 나타내 주었다. N-acetyl-L-cysteine (NAC) is a thiol-containing compound and acts as a precursor for glutathione (GSH). It behaves as an antioxidant in mammalian cells and also exerts anti-inflammatory effects. NAC is also known to affect several immune cells including eosinophils, B cells, T cells, and dendritic cells (DC) in many aspects. Even though it has been reported that NAC inhibits DC activation and shifts the immune response to Th2, these studies exhibit some contradictory results in detail and do not give any information with respect to the induction of regulatory T cells. In this study, we re-analyzed the effects of NAC on DC during their activation. We also evaluated whether it induced T cell anergy, Th1/Th2 shift, or regulatory T cells. NAC suppressed the elevation of intracellular reactive oxygen species during DC activation. In parallel, it down-regulated surface expression of CD40 and CD86, suppressed the decrease of phagocytic function, lowered the secretion of cytokines such as IL-6, IL-10, and IL-12. All these effects showed dose-dependency. Thus, it seems likely that NAC inhibited DC activation with regard to their phenotype and cytokine secretion. When we evaluated the T cell-stimulating capacity of these NAC-DC, T cell proliferation and secretion of both Th1 (IFN-γ) and Th2 cytokine (IL-5) were decreased. This implies that the T cell-stimulating activity of NAC-DC decreased without any shift to Th1 or Th2 cytokine (IL-5). The secretion of IL-10 and TGF-β in the supernatants were also decreased, which suggests that the decrease of T cell proliferation and cytokine secretion is due to the induction of T cell anergy, rather than regulatory T cells.

Nicotine Suppresses TNF-${\alpha}$ Expression in Human Fetal Astrocyte through the Modulation of Nuclear Factor-${\kappa}B$ Activation

Son, Il-Hong,Park, Yong-Hoon,Yang, Hyun-Duk,Lee, Sung-Ik,Han, Sun-Jung,Lee, Jai-Kyoo,Ha, Dae-Ho,Kang, Hyung-Won,Park, Joo-Young,Lee, Sung-Soo The Korean Society of Toxicogenomics and Toxicopro 2008 Molecular & cellular toxicology Vol.4 No.2

Parkinson's disease (PD) progresses severely by a gradual loss of dopaminergic neurons in the substantia nigra (SN). Epidemiological studies showed that the incidences of PD were reduced by smoking of which the major component, nicotine might be neuroprotective. But the function of nicotine, which might suppress the incidences of PD, is still unknown. Fortunately, recently it was reported that a glial reaction and inflammatory processes might participate in a selective loss of dopaminergic neurons in the SN. The levels of tumour necrosis factor (TNF)-${\alpha}$ synthesised by astrocytes and microglia are elevated in striatum and cerebrospinal fluid (CSF) in PD. TNF-${\alpha}$ kills the cultured dopaminergic neurons through the apoptosis mechanism. TNF-${\alpha}$ release from glial cells may mediate progression of nigral degeneration in PD. Nicotine pretreatment considerably decreases microglial activation with significant reduction of TNF-${\alpha}$ mRNA expression and TNF-${\alpha}$ release induced by lipopholysaccharide (LPS) stimulation. Thus, this study was intended to explore the role of nicotine pretreatment to inhibit the expressions of TNF-${\alpha}$ mRNA in human fetal astrocytes (HFA) stimulated with IL-$1{\beta}$. The results are as follows: HFA were pretreated with 0.1, 1, and $10{\mu}g/mL$ of nicotine and then stimulated with IL-$1{\beta}$ (100 pg/mL) for 2h. The inhibitory effect of nicotine on expressions of TNF-${\alpha}$ mRNA in HFA with pretreated $0.1{\mu}g/mL$ of nicotine was first noted at 8hr, and the inhibitory effect was maximal at 12 h. The inhibitory effect at $1{\mu}g/mL$ of nicotine was inhibited maximal at 24 h. Cytotoxic effects of nicotine were noted above $10{\mu}g/mL$ of nicotine. Moreover, Nicotine at 0.1, 1 and $10{\mu}g/mL$concentrations significantly inhibited IL-$1{\beta}$-induced TF-${\kappa}B$ activation. Collectively, these results indicate that in activated HFA, nicotine may inhibit the expression of TNF-${\alpha}$ mRNA through the pathway which suppresses the NF-${\kappa}B$ activation. This study suggests that nicotine might be neuroprotective to dopaminergic neurons in the SN and reduce the incidences of PD.

표적세포의 Nitric oxide 합성이 LAK 세포의 세포독성에 대한 예민도에 미치는 영향

박성일,박주형,이치국,김신재,최보금,곽재용,임창열,Park, Sung Il,Park, Ju Hyung,Lee, Chi Kug,Kim, Shin Chae,Choi, Bo Geum,Kwak, Jae Yong,Yim, Chang Yeol 대한면역학회 2001 Immune Network Vol.1 No.2

Background: Nitric oxide (NO), a cytotoxic molecule is produced in various tissues including tumor cells during interleukin-2 (IL-2) therapy . Lymphokine-activated killer (LAK) cells are induced during IL-2 therapy, and have cytotoxic activity against tumor cells. The current study investigated the effects of NO synthesized in target cells or exposure of target cells to NO on the sensitivity of target cells to LAK cell cytotoxicity. Methods: Cytotoxicity was measured using 4 h chromium release assays. LAK cells which were induced by a 4 day incubation of BALB/c mouse splenocytes with IL-2 (6,000 IU/mL) were employed as effector cells. RD-995 skin tumor cells originated from a C3H/HeN mouse were employed as target cells. NO synthesis in target cells was induced by a 24 h incubation of RD-995 cells with $IFN{\gamma}$ (25 U/mL), TNF (50 U/mL) and IL-1 (20 U/mL). S-nitrosyl acetylpenicillamine (SNAP), an NO donor, was used to expose target cells to NO. $N^G$-monomethyl-L-arginine (MLA) and carboxy-PTIO were added during cytotoxicity assays to inhibit NO synthesis, and to scavenge NO produced by target cells, respectively. Results: Sensitivity of NO-producing RD-995 cells to LAK cell cytotoxicity was decreased by addition of MLA and carboxy-PTIO during cytotoxicity assays. However, the two reagents had no effect on the sensitivity of non-NO-producing RD-995 cells. Pretreatment of RD-995 target cells with SNAP increased the sensitivity in comparison with untreated cells. Conclusions: Sensitivity of target cells to LAK cell cytotoxicity is increased by target cell NO synthesis or exposure to NO. Further studies are needed to evaluate whether these in vitro results have relevance to in vivo phenomena.

Silibinin polarizes Th1/Th2 immune responses through the inhibition of immunostimulatory function of dendritic cells

Lee, Jun Sik,Kim, Sang Gap,Kim, Hyung Keun,Lee, Tae-Hyung,Jeong, Young-Il,Lee, Chang-Min,Yoon, Man-Soo,Na, Yong Jin,Suh, Dong-Soo,Park, Nam Cheol,Choi, In-hak,Kim, Gi-Young,Choi, Yung Hyun,Chung, Hae Liss 2007 Journal of Cellular Physiology Vol.210 No.2

<P>Silibinin is the primary active compound in silymarin. It has been demonstrated to exert anti-carcinogenic effects and hepato-protective effects. However, the effects of silibinin on the maturation and immunostimulatory activities exhibited by dendritic cells (DCs) remain, for the most part, unknown. In this study, we have attempted to determine whether silibinin can influence surface molecule expression, dextran uptake, cytokine production, capacity to induce T-cell differentiation, and the signaling pathways underlying these phenomena in murine bone marrow-derived DCs. Silibinin was shown to significantly suppress the expression of CD80, CD86, MHC class I, and MHC class II in the DCs, and was also associated with impairments of LPS-induced IL-12 expression in the DCs. Silibinin-treated DCs proved highly efficient with regard to Ag capture via mannose receptor-mediated endocytosis. Silibinin also inhibited the LPS-induced activation of MAPKs and the nuclear translocation of the NF-κB p65 subunit. Additionally, silibinin-treated DCs evidenced an impaired induction of Th1 response, and a normal cell-mediated immune response. These findings provide new insight into the immunopharmacological functions of silibinin, especially with regard to their impact on the DCs. These findings expand our current understanding of the immunopharmacological functions of silibinin, and may prove useful in the development of therapeutic adjuvants for acute and chronic DC-associated diseases. J. Cell. Physiol. 210: 385–397, 2007. © 2006 Wiley-Liss, Inc.</P>

만성폐쇄성폐질환의 중증도와 폐고혈압 및 폐성심으로 진행과의 상관관계

김형호,박철진,이준,장광표,하성일,이재록,하재화,권세훈,권용운,윤성호,이승일 朝鮮大學校 附設 醫學硏究所 2007 The Medical Journal of Chosun University Vol.32 No.2

Background: From many previous studies, Pulmonary hypertension is the known independent predictive factor of the mortality in COPD. Also pulmonary hypertension is the major cardiovascular complication of COPD and is associated with the progression to cor pulmonale and poor prognosis. Author want to analyze the correlation between pulmonary hypertension and the severity of COPD which are classified by forced expiratory volume in one second, and the extent of progression to corpulmonale. Methods: Retrospectively we investigated the medical records of 118 patients with COPD who had pulmonary function test and echocardiogaphy more than one times during one-year follow-up (from June, 2005 to May, 2006) at respiratory division in chosun university hospital, and then 50 patients were enrolled in this study. We classified the severity from FEVl in pulmonary function test based on the GOLD guideline, also this was comparably analyzed with RVSP, RVIDd, Visual Grading from echocardiography. Results: 16 patients out of 50 were classified as moderate severity, 25 patients were severe, and 9 patients were very severe group. RVSP was higher in more severe groups than less severe groups but when it comes to pulmonary hypertension that RVSP is over 35 mmHg, there was no valid difference lies in those groups. As FEVl decreases RVSP and RVIDd increases, and observed relationship between RVSP which was classified as below 35 mm and above 35 mm groups and visual grading which was classified as normal and dilatated groups revealed valid correlation, Conclusion: As pulmonary function decreases, progression to pulmonary hypertension and cor pulmonale increases but there was no remarkable difference of prevalence in above moderate severity groups. 연구배경 폐고혈압은 이전의 많은 연구에서 만성폐쇄성폐질환에서 독립적인 사망의 예측인자로 알려져 있다. 또한 폐고혈압은 만성폐쇄성폐질환의 주요한 심혈관계 합병증이며, 폐성심으로의 진행 및 불량한 예후와도 관련되어 있다. 이에 저자는 폐고혈압과 1초간 노력성호기량으로 분류되는 만성폐쇄성폐질환의 중증도 및 폐성심으로의 진행 정도를 비교 분석하여 이들의 상관관계를 밝혀보고자 한다. 방법 2005년 6월부터 2006년 5월까지 1년 동안 본 병원 호흡기 내과에서 폐기능검사와 심장초음파 검사를 각각 1회 이상 시행한 적이 있는 118명에 한하여 의무기록을 후향적으로 조사하여 이 중에서 50명을 대상으로 하였다. 폐기능검사 시행 결과 얻은 1초간 노력성호기량을 바탕으로 GOLD guideline에 따라 중증도를 분류하였으며 이를 심초음파 시행 결과 얻은 우심실수축기압, 확장기말 우심실내부간격, 시각등급과 비교분석하였다. 결과 대상 환자 50명중 16명은 중등증, 25명은 중증, 9명은 최고중증 그룹으로 분류되었다. 우심실수축기압은 중증도가 높은 그룹에서 낮은 그룹에 비해 더 높게 나타났으나 폐고혈압에 해당하는 우심실수축기압이 35 mmHg이상인 환자에 있어사는 각 그룹간에 유의한 차이를 보이지 않았으며, 확장기말 우심실내부간격, 시각등급 또한 중증도와 유의한 차이를 보이지 안항ㅆ다. 1초간 노력성호기량이 감소함에 따라서는 우심실수축기압, 시각등급은 증가하였으며 우심실수축기압을 35mmHg 미만과 이상인 그룹으로, 시각등급을 정상과 확장이 있는 그룹으로 분류하여 비교한 결과에서는 유의한 상관관계를 나타냈다. 결론 폐기능이 감소할수록 페고혈압 및 폐성심으로의 진행이 증가하였으나 폐기능검사에서 중등도 이상의 그룹에서 유병률의 차이는 크지 않았다.

생쥐의 B 세포에서 anti-CD40과 rIL-4로 유도된 싸이토카인 생산에 대한 자오가의 효과

성일창 ( Il Chang Sung ),김형환 ( Hyung Hwan Kim ),안덕균 ( Duk Kyun Ahn ),이용섭 ( Yong Sup Lee ),서영배 ( Young Bae Seo ),최호영 ( Ho Young Choi ) 대한본초학회 2003 大韓本草學會誌 Vol.18 No.2

N/A Objectives : In order to study the anti-allegy effect of water extract of Acanthopanacis senticosi Radix (ASR) on the B-cells from healthy Balblc mice. Methods : The cytotoxicity of ASR was measured with the murine normal lung fibroblast cells by modified SRB assay. And the murine splenic B-cells was stimulated with anti-CD40 mAb and rIL4. The various cytokines related with allergy were measured by flow-cytometry and by RT-PCR with electophoresis. Results : The anti-allegy effects to ASR were identified and observed. The cytotoxicity of ASR on mouse lung fibroblast cells showed no significant activities. ASR had inhibitory effect on CD23+, CD69+, and IgE expression by ASR with anti-CD40 mAb plus rL-4-stimulated murine splenic B-cells. ASR had inhibitory effect on cytokines (E-lb, IL-4, IL-6, IL-10, TNF-a, TGF-81, INF-Y) and transcript expression and IgE production by ASR with anti-CD40 mAb plus rIL-4-stimulated murine splenic B-cells. Conclusion : We concluded that ASR showed anti-allegy effect on murine splenic B-cells.

삼백초(三白草)의 소염작용(消炎作用)에 대(對)한 실험적(實驗的) 연구(硏究)

변형국 ( Hyung Kuk Byun ),신용완 ( Yong Wan Shin ),김의일 ( Eui Il Kim ),김수민 ( Su Min Kim ),이정은 ( Jung Eun Lee ),유동열 ( Dong Youl Yoo ) 대한한방부인과학회 2005 大韓韓方婦人科學會誌 Vol.18 No.4

Purpose: The purpose of this research was to investigate the effects of Saurui Herba Seu Rhizoma(SHSR) on Anti-inflammatory properties in Raw264.7 cell line and murine models of inflammation. Methods: To investigate the effects of Saurui Herba Seu Rhizoma(SHSR) on anti-inflammation, we study cytotoxicity effects of SHSR on Mouse Lung Fibroblast Cells and Peritoneal Macrophages, Inhibitory effects of SHSR on the nitric oxide (NO) release, the ROS production, and the interleukin-6 production. Results: The cytotoxicity of SHSR on mouse lung fibroblast Cells and Raw264.7 cell line was not observed. SHSR in RAW264.7 cell line inhibited IL-1β, IL-6 mRNA gene expression depending upon the concentrations of extract and inhibited IL-18 mRNA gene expression at 100 ㎍/㎖ of extract. SHSR in RAW264.7 cell line inhibit COX-2 mRNA gene expression at 100, 10 ㎍/㎖ of extract. SHSR in RAW264.7 cell line inhibited NOS-Ⅱ mRNA gene expression depending upon the concentrations of extract. SHSR in RAW264.7 cell line didn``t inhibit TNF-α mRNA gene expression. SHSR in RAW264.7 cell line decreased IL-6 production depending upon the concentrations of extract. SHSR in RAW264.7 cell line decreased ITNF-α production according to the concentrations of extract. SHSR in RAW264.7 cell line inhibited NO release specially SHSR 100, 10 ㎍/㎖ concentrations of extract. SHSR inhibit ROS production depending upon the concentrations of extract. Conclusion: These results suggest that SHSR can be used treating a lot of women disease caused by inflammation.