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OMC-2010 추출물이 마우스의 비장세포 cytokine 생성에 미치는 영향
배기상 ( Gi Sang Bae ),박경철 ( Kyoung Chel Park ),최선복 ( Sun Bok Choi ),조일주 ( Il Joo Jo ),서상완 ( Sang Wan Seo ),김종진 ( Jong Jin Kim ),신용국 ( Yong Kook Shin ),김민선 ( Min Sun Kim ),박규환 ( Kyu Hwan Park ),김현식 ( Hyu 대한본초학회 2012 大韓本草學會誌 Vol.27 No.5
Objective : This study was performed to estimate the effects of OMC-2010 extract on cytokine production in mouse spleen cells. Methods : Mouse spleen cells were pre-treated with ethanol and water extract of OMC-2010 for 1 h, then stimulated with lipopolysaccharide (LPS, 1 μg/ml) for 48 h. Then the cells were harvested for real-time reverse transcription polymerase chain reaction to detect cytokines. Results : OMC-2010 ethanol extract significantly inhibited the LPS-induced interleukin (IL)-1beta, tumor necrosis factor (TNF)-alpha and IL-5 mRNA expressions, but not shown such changes in IL-6, IL-4, IL-13. OMC-2010 water extract significantly inhibited the LPS-induced TNF-alpha, and IL-5 mRNA expressions, but not shown such changes in IL-1beta, IL-6, IL-4, IL-13. Conclusions : Theses results could suggest that both ethanol and water OMC-2010 extract could inhibit the TNF-alpha and IL-5 mRNA expression.
Jung, In Duk,Lee, Min-Goo,Chang, Jeong Hyun,Lee, Jun Sik,Jeong, Young-Il,Lee, Chang-Min,Park, Won Sun,Han, Jin,Seo, Su-Kil,Lee, Sang Yong,Park, Yeong-Min Williams Wilkins 2009 JOURNAL OF IMMUNOLOGY Vol.182 No.5
<P>Suppression of an excessive systemic inflammatory response is a promising and potent strategy for treating endotoxic sepsis. Indoleamine 2,3-dioxygenase (IDO), which is the rate-limiting enzyme for tryptophan catabolism, may play a critical role in various inflammatory disorders. In this study, we report a critical role for IDO in the dysregulated immune response associated with endotoxin shock. We found that IDO knockout (IDO(-/-)) mice and 1-methyl-D-tryptophan-treated, endotoxin-shocked mice had decreased levels of the cytokines, TNF-alpha, IL-6, and IL-12, and enhanced levels of IL-10. Blockade of IDO is thought to promote host survival in LPS-induced endotoxin shock, yet little is known about the molecular mechanisms that regulate IDO expression during endotoxin shock. In vitro and in vivo, IDO expression was increased by exogenous IL-12, but decreased by exogenous IL-10 in dendritic cells and splenic dendritic cells. Interestingly, whereas LPS-induced IL-12 levels in serum were higher than those of IL-10, the balance between serum IL-12 and IL-10 following challenge became reversed in IDO(-/-)- or 1-methyl-D-tryptophan-treated mice. Our findings demonstrate that the detrimental immune response to endotoxin shock may occur via IDO modulation. Restoring the IL-12 and IL-10 balance by blocking IDO represents a potential strategy for sepsis treatment.</P>
OMC-2010 구성약재 배합추출물 투여가 Ovalbumin으로 유도한 마우스 알레르기성 기관지 천식에 미치는 영향
조일주 ( Il Joo Jo ),배기상 ( Gi Sang Bae ),최선복 ( Sun Bok Choi ),송호준 ( Ho Joon Song ),박성주 ( Sung Joo Park ),서상완 ( Sang Wan Seo ),옥주안 ( Joo An Ok ),김민선 ( Min Sun Kim ),백선종 ( Sun Jong Baek ),배익현 ( Ik Hyun Bae 대한본초학회 2013 大韓本草學會誌 Vol.28 No.5
Objectives: We recently have reported that constituents of OMC-2010 have an immuno-modulatory effects via inhibiting tumor necrosis factor (TNF)-alpha and interleukin (IL)-5. In this study, based on previous data, we investigated the effects of combinations with each OMC constituents on splenocyte cytotoxicity, cytokine productions, and ovalbumin (OVA) induced experimental allergic asthma. Methods: Mouse splenocytes were pre-treated with ethanol extract of constituents of Rehmannia glutinosa (RG), Pinellia ternata (PT), Schisandra chinensis (SC). We made 4 combinations using RG, PT, and SC (A;1:1:1, B;2:1:1, C;1:2:1, D;1:1:2). The cells were pretreated with A, B, C, or D for 1 h, then stimulated with lipopolysaccharide (LPS, 1 ㎍/ml) for 48 h. Then the cells were harvested for real-time reverse transcription polymerase chain reaction to detect cytokine productions. Then using effective combination from RG, PR and SC, we administrated the combination orally, then challenged with OVA to induce asthma. Then we analyzed the airway hyper-reactivity (AHR), lung histology and lung TNF-α and IL-5 mRNA. Results: A. B. C. and D did not showed significant cytotoxicity on splenocytes. Pre-treatment of A inhibited the expression of TNF-α and IL-5 significantly, but not B, C, and D. In experimental asthma, administration of A significantly inhibited the increase of AHR, lung damage, TNF-α and IL-5 expression. Conclusions: Theses results could suggest that inhibitory effects of the ideal combination with RG, PT and SC (1:1:1) could be applied to treatment of asthma and study of asthma mechanisms.
노성일 ( Sung Il Noh ),김상돈 ( Sang Don Kim ),박성철 ( Sung Cheul Park ),서병윤 ( Byung Yun Seo ),염승룡 ( Seung Ryong Yeom ),권영달 ( Young Dal Kwon ),신병철 ( Byung Cheul Shin ),송용선 ( Yung Sun Song ) 한방재활의학과학회 2005 한방재활의학과학회지 Vol.15 No.2
목적 : 방풍은 임상적으로 관절염을 포함한 다양한 염증성 질환 치료제로 사용되어 왔다. 본 연구에서는 인간 비만세포를 이용하여 세포 독성에 영향을 주지 않는 농도에서 방풍의 항염 효과 및 그 기전을 검토했다. 방법 : 인간의 HMC-1세포를 IMDM에서 페니실린, 스트렙토마이신, 모노티오글리세린를 첨가하여 배양하고 방풍추출액을 투여하였다. 그 다음 MTT, ELISA, RT-PCR, 세포내 칼슘측정, 핵단백분석을 이용하여 TNF-α, IL-6, IL-8 각각의 형성과 mRNA발현, 세포내 칼슘 수준, NF-κB 발현에 대한 방풍추출액의 반응을 측정하고 통계처리 하였다. 결과 : 방풍은 PMA와 calcium ionophore A23187로 활성화된 비만세포에서 세포내 칼슘 수준과 NF-κB, TNF-α와 IL-6의 발현을 억제 시켰고 RT-PCR을 이용한 mRNA 발현에서 TNF-α와 IL-6의 발현을 억제하였다. 결론 : 방풍은 비만세포내 칼슘 수준 및 NF-κB의 활성을 억제하고 염증성 세포 활성 물질인 TNF-α와 IL-6의 분비도 억제하여 항염 효과를 나타냄을 암시하고 있다.
진통산(痛散)이 흰쥐의 adjuvant 유발 관절염 및 척수내 C-fos 발현에 미치는 영향
손동우 ( Dong Woo Son ),김순중 ( Sun Jung Kim ),서일복 ( Il Bok Seo ) 한방재활의학과학회 2005 한방재활의학과학회지 Vol.15 No.3
Objectives : This study was carried out to investigated the anti-pathogenetic and curative effects of Jintong-san(Chentong-san) on Complete Freund`s Adjuvant(CFA) induced arthritis in rats. Methods : In experiment, Thirty male rats were divided into non-treated normal group(n=12), control group(n=12) is distilled water treated for 15 days after onset of arthritis by CFA, treated group(n=6) is Jintong-san(Chentong-san) treated for 15 days after onset of arthritis by CFA. Body weight, paw edema volume, and thickness of ankle joint were measured at 0, 5, 10, 15 days after treatment. At 15 days after treatment, IL-1β, IL-6 and PGE2 level in Paw Exudate were analysed for anti-inflammatory effect, C-fos immunoreactive cells measurement for analgesic effect, and histopathological examination was performed on the ankle joint. Results : Paw edema volume, thickness of ankle joint, IL-1β, IL-6, PGE2, C-fos immunoreactive cells number of treated group was significantly decreased compared with control group and histopathologically, destructive lesions of articular cartilage and subchondral bony tissue, and degree of fibrous ankylosis in treated group were alleviated compared with those of control group. Conclusions : These results indicated that Jintong-san(Chentong-san) has inhibitory effects on the progression of CFA arthritis in rats, by it`s lowering effects on the secretion of IL-1β, IL-6 and PGE2, and analgesic effect by C-fos immunoreactive cells decrease.
삼황사심탕(三黃瀉心湯)이 난황 알부민으로 유도된 알레르기 Mouse모델에서 항알레르기 효과
최종환 ( Chong Hwan Choi ),금선오 ( Seo Oh Keum ),이세원 ( Se Won Lee ),김일현 ( Il Hyun Kim ),이하일 ( Ha Il Lee ),송용선 ( Yung Sun Song ) 한방재활의학과학회 2014 한방재활의학과학회지 Vol.24 No.3
Objectives In this study, we investigated the inhibitory effects of Samhwangsasim-tang (S.H) on the allergic response caused by ovalbumin(OVA) sensitization and challenge in BALB/c mice. Methods The experimental animals were divided into five groups; 1) normal as negative control, 2) OVA-sensitized mice, 3) OVA-sensitized mice treated with 200 mg/kg of S.H 200, 4) OVA-sensitized mice treated with 400 mg/kg of S.H 400, and 5) OVA-sensitized mice treated with 5 mg/kg of Dexamethasone (Dex). Antigen sensitization for allergic mouse model was performed with twice injection of OVA for 2 weeks. After secondary injection, S.H was administrated orally into mice every day for 13 days and the inhibitory effect of S.H on allergic responses was evaluated. Results Treatment of S.H into allergic mice reduced significantly ear edema and infiltration of immune cells in ear tissues induced with OVA challenge in a dose-dependent manner. S.H reduced significantly the serum levels of Total Immunoglobulin(Ig)G and IgE, and particularly inhibited the production of OVA-specific IgE, but not OVA-specific IgG. The serum level of proinflammatory cytokine TNF-α and Th2-associated cytokine IL-4 also were significantly decreased by S.H adminstration in a dose denpendent manner. S.H attenuated OVA-induced secretion of IFN-γ, but not IL-12 which is a cytokine inducing the development of Th1 cells. It also reduced significantly the secretion of IL-4, which is a cytokine inducing the development of Th2 cells, after splenocytes were stimulated with OVA. However the secretion of IL-5 and IL-13 was influenced weakly or a little. Conclusions These results indicate that S.H could reduce the allergic response through inhibition of antigen-specific IgE and Th2-inducing cytokines. It suggest that S.H may be available clinically for the treatment of allergic patients. (J Korean Med Rehab 2014;24(3): 71-85)
Yang, Jae-Wook,Jung, Won-Kyo,Lee, Chang-Min,Yea, Sung Su,Choi, Yung Hyun,Kim, Gi-Young,Lee, Dae-Sung,Na, Giyoun,Park, Sae-Gwang,Seo, Su-Kil,Choi, Jung Sik,Lee, Young-Min,Park, Won Sun,Choi, Il-Whan Informa Healthcare USA, Inc. 2014 IMMUNOPHARMACOLOGY AND IMMUNOTOXICOLOGY Vol.36 No.5
<P><I>Context</I>: Expression of various inflammatory mediators in corneal fibroblasts contributes to corneal inflammation.</P><P><I>Objective</I>: The purpose of this study was to assess the possible effects of caffeic acid phenethyl ester (CAPE) on the expression of inflammatory mediators during an inflammatory response in human corneal fibroblasts.</P><P><I>Materials and methods</I>: The levels of interleukin (IL)-6, monocyte chemotactic protein (MCP)-1, and intercellular adhesion molecule-1 (ICAM-1) from IL-1β-exposed human corneal fibroblasts were measured with enzyme-linked immunosorbent assays (ELISA). The regulatory mechanisms of CAPE on cellular signaling pathways were examined using Western blot and electrophoretic mobility shift assays. A functional validation was carried out by evaluating the inhibitory effects of CAPE on neutrophil and monocyte migration <I>in vitro</I>.</P><P><I>Results</I>: CAPE inhibited the expression of IL-6, MCP-1 and ICAM-1 induced by the pro-inflammatory cytokine IL-1β in corneal fibroblasts. The activation of AKT and NF-κB by IL-1β was markedly inhibited by CAPE, whereas the activity of mitogen-activated protein kinases (MAPKs) was not affected. CAPE significantly suppressed the IL-1β-induced migration of differentiated (d)HL-60 and THP-1 cells.</P><P><I>Discussion</I>: These anti-inflammatory effects of CAPE may be expected to inhibit the infiltration of leukocytes into the corneal stroma <I>in vivo</I>.</P>
LPS로 유도한 RAW 264.7 세포의 염증반응에서 자초(紫草)의 항염증 효과
최선복 ( Sun Bok Choi ),배기상 ( Gi Sang Bae ),조일주 ( Il Joo Jo ),박경철 ( Kyoung Chel Park ),서승희 ( Seung Hee Seo ),김동구 ( Dong Goo Kim ),신준연 ( Joon Yeon Shin ),곽태신 ( Tae Sin Gwak ),이정현 ( Jung Hyun Lee ),이금산 ( G 대한본초학회 2013 大韓本草學會誌 Vol.28 No.2
Objective: Lithospermum Erythrorhizon (LE) has been used as an anti-bacterial and anti-inflammatory agent. However, it is unclear that LE aqueous extract could show the anti-inflammatory effects in RAW 264.7cells. The purpose of this study was to investigate the anti-inflammatory effect of aqueous extract from LE on lipopolysaccharide (LPS) - induced inflammatory response. Methods: To measure out the cytotoxicity of LE, we performed the MTT assay. To evaluate the anti-inflammatory effects of LE, we examined the inflammatory mediators such as nitric oxide (NO), prostaglandin E2 (PGE2) and pro-inflammatory cytokines (tumor necrosis factor (TNF)-a, interleukin, (IL)-1β and (IL)-6) on RAW 264.7 cells. We also examined molecular mechanisms such as mitogen-activated protein kinases (MAPKs) and nuclear factor-B (NF-κB) activation by western blot. Results : Aqueous Extract from LE itself did not have any cytotoxic effect in RAW 264.7 cells. Aqueous extract from LE inhibited LPS-induced productions of inflammatory mediators such as NO, PGE2, and pro-inflammatory cytokines including TNF-a, IL-1β and IL-6 in RAW 264.7cells. In addition, LE inhibited the phosphorylation of p38 kinases (p38), c-Jun NH2-terminal kinase (JNK), and NF-κB activation in RAW 264.7 cells. Conclusion : LE down-regulated LPS-induced production of inflammatory mediators through the inhibition of p38, JNK and NF-κB activation. Taken together, these results could provide the evidence for the anti-inflammatory effects of LE. Therefore, LE may be a novel target in the management of inflammation and help to support a potential strategy for prevention and therapy of inflammatory diseases.
LPS로 유도한 대식세포의 염증반응에서 우슬의 항염증 효과
김민선 ( Min Sun Kim ),정진수 ( Jin Soo Jeong ),이혜윤 ( Hye Youn Lee ),주영승 ( Young Sung Ju ),배기상 ( Gi Sang Bae ),서상완 ( Sang Wan Seo ),조일주 ( Il Joo Cho ),박성주 ( Sung Joo Park ),송호준 ( Ho Joon Song ) 대한본초학회 2011 大韓本草學會誌 Vol.26 No.2
Objectives: Achyranthes japonica (AJ ) has been used as an anti-bacterial and anti-inflammatory agent. However, it is unclear that AJ could show the anti-inflammatory effects in macrophages. In this experiment, we studied whether AJ could inhibit the inflammatory responses in macrophages. Methods: To measure out the cytotoxicity of AJ, we performed the MTT assay. We evaluated the nitric oxide (NO) production, and cytokine production such as interleukin (IL)-1b, IL-6 and tumor necrosis factor (TNF)-a. We also investigated the cellular mechanims such as mitogen activated protein kinases (MAPK)s and nuclear factor kappa B (NF-kB). Results: AJ inhibited lipopolysaccharide (LPS)-induced NO production. AJ also inhibited production levels of IL-1b, IL-6 and TNF-a in LPS-stimulated macrophage. Finally, western blot analysis showed that AJ treatment inhibited the activation of p38 but not of extracellular signal-regulated kinase, c-jun NH2-terminal kinase and NF-kB. Conclusions: These results showed that AJ down-regulated the inflammatory response via p38 in macrophages, which suggest that AJ could be a candidate on treating inflammatory diseases.
Lee, Young-Sun,Yi, Hyon-Seung,Suh, Yang-Gun,Byun, Jin-Seok,Eun, Hyuk Soo,Kim, So Yeon,Seo, Wonhyo,Jeong, Jong-Min,Choi, Won-Mook,Kim, Myung-Ho,Kim, Ji Hoon,Park, Keun-Gyu,Jeong, Won-Il Korean Society for Molecular and Cellular Biology 2015 Molecules and cells Vol.38 No.11
Retinols are metabolized into retinoic acids by alcohol dehydrogenase (ADH) and retinaldehyde dehydrogenase (Raldh). However, their roles have yet to be clarified in hepatitis despite enriched retinols in hepatic stellate cells (HSCs). Therefore, we investigated the effects of retinols on Concanavalin A (Con A)-mediated hepatitis. Con A was injected into wild type (WT), Raldh1 knockout ($Raldh1^{-/-}$), $CCL2^{-/-}$ and $CCR2^{-/-}$ mice. For migration study of regulatory T cells (Tregs), we used in vivo and ex vivo adoptive transfer systems. Blockade of retinol metabolism in mice given 4-methylpyrazole, an inhibitor of ADH, and ablated Raldh1 gene manifested increased migration of Tregs, eventually protected against Con A-mediated hepatitis by decreasing interferon-${\gamma}$ in T cells. Moreover, interferon-${\gamma}$ treatment increased the expression of ADH3 and Raldh1, but it suppressed that of CCL2 and IL-6 in HSCs. However, the expression of CCL2 and IL-6 was inversely increased upon the pharmacologic or genetic ablation of ADH3 and Raldh1 in HSCs. Indeed, IL-6 treatment increased CCR2 expression of Tregs. In migration assay, ablated CCR2 in Tregs showed reduced migration to HSCs. In adoptive transfer of Tregs in vivo and ex vivo, Raldh1-deficient mice showed more increased migration of Tregs than WT mice. Furthermore, inhibited retinol metabolism increased survival rate (75%) compared with that of the controls (25%) in Con A-induced hepatitis. These results suggest that blockade of retinol metabolism protects against acute liver injury by increased Treg migration, and it may represent a novel therapeutic strategy to control T cell-mediated acute hepatitis.