• IMMUNE NETWORK
• /
• 제2권1호
• /
• pp.25-34
• /
• 2002

Background: Rheumatoid arthritis (RA) is a chronic inflammatory disease characterized by synovial hyperplasia and joint destruction. The synovial fibroblasts express cell adhesion molecules and have a role in adhesive interation with inflammatory cells in synovial tissue. It has been suggested that hypoxic conditioins are thought to exist in arthritic joints, and several studies indicate that reactive oxygen species (ROS) produced in hypoxic condition can initiate events that lead to pro-adhesive changes via increased expression of adhesion molecules. So, this study wsa designed to examine whether antioxidant can inhibit hypoxia-induced expression of ICAM-1 in cultured human synovial fibroblasts. Methods: Synovial fibroblasts were isolated from synovial tissue in patients with RA and cultured at hypoxic condition. Antioxidant, PDTC (pyrrolidine dithiocarbamate) were pre-treated for an hour before the hypoxic culture and synovial fibroblasts were harvested at 0, 6, 12, 24, 48 hours time points. Cell surface ICAM-1 expression in synovial fibroblasts was examined by the flow cytometric analysis. To analyse the expression of ICAM-1 mRNA, reverse-transcriptase polymerase chain reaction (RT-PCR) was performed. The levels of cytokines in culture supernatants were measured by ELISA, and activation of NF-${\kappa}B$ was analysed by electrophoretic mobility shift assay. The adhesive reaction between synovial fibroblasts and lymphocytes was assayed by measurement of fluorescent intensity of BCECF-AM in lymphocytes. Results: Hypoxic stimuli up-regulated the ICAM-1 expression as well as the adhesive interaction of human synvial fibroblasts to lymphocytes in a time-dependent manner, and PDTC inhibited hpyoxia-induced ICAM-1 expression and cell-cell interaction. PDTC also inhibited the hypoxia-induced activation of intracellular transcription factor, NF-${\kappa}B$. PDTC decreased the amount of hypoxia-induced production of IL-$1{\beta}$ and TNF-${\alpha}$. Conclusion: These studies demonstrate that PDTC inhibit the hypoxia-induced expression of the adhesion molecule, ICAM-1 and activation of NF-${\kappa}B$ in cultured human synovial fibroblasts.

• 대한한의학회지
• /
• 제26권1호
• /
• pp.26-36
• /
• 2005

Objective : Many traditional herbal remedies exhibit several beneficial effects including anti-inflammation. Euonymus alatus (Thunb.) Sieb (EA), known as Gui jun woo in Korea, has long been used in folk medicine to regulate Qi (bodily energy) and blood circulation, relieve pain, eliminate stagnant blood, and treat dysmenorrhea in oriental countries. The exact mechanism of the anti-inflammatory action of Euonymus alatus (Thunb.) Sieb (EA), however, has not been determined. Methods: Since there is increasing evidence that nitric oxide (NO) plays a crucial role in the pathogenesis of inflammatory diseases, this study was undertaken to address whether the methanol (MeOH) extract and its fractions of the bark of EA could modulate the expression of inducible NO synthase (iNOS) in thioglycollate-elicited murine peritoneal macrophages and murine macrophage cell line, RA W264.7 cells. Results: Stimulation of the peritoneal macrophages and RAW264.7 cells with $interferon-\gamma\;(IFN-\gamma)$ and lipopolysaccharide (LPS) resulted in increased production of NO in the medium. However, the butanol (BuOH) fraction of the MeOH extract of EA barks showed marked inhibition of NO synthesis in a dose-dependent manner. The inhibition of NO synthesis was reflected in the decreased amount of iNOS protein, as determined by Western blotting. The BuOH fraction did not affect the viability of RA W264.7 cells, as assessed by methylthiazol-2-yl-2, 5-diphenyl tetrazolium bromide (MTT) assay; rather, it reduced endogenous NO-induced apoptotic cell death via inhibition of NO synthesis in RAW264.7 cells. On the other hand, the MeOH and BuOH fraction showed no inhibitory effect on the synthesis of NO by RAW264.7 cells, when iNOS was already expressed by the stimulation with $IFN-\gamma$ and LPS. Conclusion: Collectively, these results demonstrate that the MeOH and BuOH fraction inhibits NO synthesis by inhibition of the induction of iNOS in murine macrophages.

• Journal of Chest Surgery
• /
• 제54권1호
• /
• pp.9-16
• /
• 2021

Background: The deposition of monomeric C-reactive protein (mCRP) in the myocardium aggravates ischemia-reperfusion injury (IRI) and myocardial infarction. Ischemic preconditioning (IPC) is known to protect the myocardium against IRI. Methods: We evaluated the effects of IPC on myocardium upon which mCRP had been deposited due to IRI in a rat model. Myocardial IRI was induced via ligation of the coronary artery. Direct IPC was applied prior to IRI using multiple short direct occlusions of the coronary artery. CRP was infused intravenously after IRI. The study included sham (n=3), IRI-only (n=5), IRI+CRP (n=9), and IPC+IRI+CRP (n=6) groups. The infarcted area and the area at risk were assessed using Evans blue and 2,3,5-triphenyltetrazolium staining. Additionally, mCRP immunostaining and interleukin-6 (IL-6) mRNA reverse transcription-polymerase chain reaction were performed. Results: In the IRI+CRP group, the infarcted area and the area of mCRP deposition were greater, and the level of IL-6 mRNA expression was higher, than in the IRI-only group. However, in the IPC+IRI+CRP group relative to the IRI+CRP group, the relative areas of infarction (20% vs. 34%, respectively; p=0.079) and mCRP myocardial deposition (21% vs. 44%, respectively; p=0.026) were lower and IL-6 mRNA expression was higher (fold change: 407 vs. 326, respectively; p=0.376), although the difference in IL-6 mRNA expression was not statistically significant. Conclusion: IPC was associated with significantly decreased deposition of mCRP and with increased expression of IL-6 in myocardium damaged by IRI. The net cardioprotective effect of decreased mCRP deposition and increased IL-6 levels should be clarified in a further study.

• Journal of Microbiology and Biotechnology
• /
• 제9권1호
• /
• pp.106-112
• /
• 1999

The therapeutic potential of phosphodiesterase 4(PDE4) inhibitors in inflammatory diseases including some autoimmune diseases has been explored recently with some hopeful results. These PDE4 inhibitors are thought to show their anti-inflammatory effect by down-regulating tumor necrosis factor-a (TNF-$\alpha$) production in lymphocytes and macrophages. A high concentration of TNF-$\alpha$has been found in rheumatoid arthritis (RA) synovium and reducing TNF-$\alpha$using biological agents was proven to be an effective RA treatment. To test the possibility of using PDE4 inhibitors for RA treatment, the effects of a newly synthesized PDE4 inhibitor, DWP205505, on TNF-$\alpha$ and IL-10 production was tested in cells isolated from normal peripheral blood and rheumatoid arthritis synovial fluid. Cytokine production was assayed at the protein level by sandwich enzyme-linked immunosorbent assay (ELISA) and at the mRNA expression level by semi-quantitative RT-PCR. Another PDE4 inhibitor, RP73401, was used for comparison. DWP205505 and RP73401 had no harmful effect on cell viability up to 10 $\mu$M concentration during the 24 h culture period. DWP205505 as well as RP73401 significantly reduced TNF-$\alpha$ secretion from lipopolysaccharide (LPS)-stimulated peripheral blood mononuclear cells (pBMC) and synovial fluid mononuclear cells (SFMC). The effect of DWP205505 or RP73401 treatment on the mRNA expression of TNF-$\alpha$ was also studied in LPS-stimulated PBMC and SFMC. TNF-$\alpha$ mRNA expression was increased by LPS stimulation and both of the PDE4 inhibitors suppressed TNF-$\alpha$ mRNA expression. For interleukin-l0 (IL-l0), a little different results were obtained from PBMC and SFMC; IL-l0 secretion was unaffected by LPS stimulation and only minimally affected by both of the PDE4 inhibitors in PBMC. In unstimulated SFMC, DWP205505 and RP73401 slightly enhanced IL-10 secretion, while they reduced IL-l0 secretion from LPS-stimulated SFMC where IL-l0 secretion was a lot higher than unstimulated SFMC. These results suggest that the newly synthesized PDE4 inhibitor DWP205505 may have anti-rheumatoid arthritis activity.

• IMMUNE NETWORK
• /
• 제9권6호
• /
• pp.255-264
• /
• 2009

Background: Chronic low grade inflammation is closely linked to type II diabetes, obesity, and atherosclerosis. Macrophages play a key role in the regulation of pro- or anti-inflammatory actions at the lesion sites of disease. Components of cordyceps militaris, cordycepin and adenosine, have been used for the modulation of inflammatory diseases. The effects of cordycepin in the modulation of macrophages have yet to be be elucidated. We investigated the effects of cordycepin and adenosine on the morphological changes of macrophages under the inflammatory condition of LPS and an anti-inflammatory condition involving high concentrations of adenosine. Methods: We confirmed the mRNA levels of the M1/M2 cytokine genes through RT-PCR and morphological change. Results: LPS-activated macrophages returned to their inactivated original shape, i.e., they looked like naive macrophages, through the treatment with high concentrations of cordycepin ($40{\mu}g/ml$). LPS and adenosine activated macrophages also returned to their original inactivated shapes after cordycepin treatment; however, at relatively higher levels of cordycepin than adenosine. This change did not occur with relatively low concentrations of cordycepin. Adenosine down-regulated the gene expression of M1 cytokines (IL-$1{\beta}$, TNF-${\alpha}$) and chemokines (CX3CR1, RANTES), such as cordycepin. Additionally, M2 cytokines (IL-10, IL-1ra, TGF-${\beta}$) were up-regulated by both cordycepin and adenosine. Conclusion: Based on these observations, both cordycepin and adenosine regulated the phenotypic switch on macrophages and suggested that cordycepin and adenosine may potentially be used as immunomodulatory agents in the treatment of inflammatory disease.

• 셀메드
• /
• 제9권1호
• /
• pp.5.1-5.4
• /
• 2019

Atopic dermatitis (AD) is an allergic and inflammatory skin. Recently, the limitations and side effects of drug therapy, and possibility of alternative therapies, such as music therapy are emerging in the treatment of AD. Thus, the present study determined whether traditional Korean music, Daegeum Sanjo, regulates AD symptoms by comparing the rhythm, Jinyangjo-jangdan and Jungmori-jangdan in an AD-like murine model. Jinyangjo-jangdan and Jungmori-jangdan of Daegeum Sanjo reduced the duration of scratching behavior increased by DNFB challenge. Jinyangjo-jangdan and Jungmori-jangdan of Daegeum Sanjo attenuated clinical symptoms. However, Jinyangjo-jangdan and Jungmori-jangdan of Daegeum Sanjo did not inhibit IgE, histamine, interleukin (IL)-4, IL-6, or thymic stromal lymphopoietin levels in serum or AD-like skin lesions. In conclusion, the present study suggests that it is possible for Jinyangjo-jangdan and Jungmori-jangdan of Daegeum Sanjo to ameliorate AD symptoms. However, further study is needed to clarify significant mechanisms of Jinyangjo-jangdan and Jungmori-jangdan of Daegeum Sanjo therapy for AD symptoms.

• The Journal of Korean Physical Therapy
• /
• 제21권2호
• /
• pp.103-108
• /
• 2009

Purpose: Electrical stimulation is one of several treatments recommended for RA patients. Electrical stimulation of RA patients, reduces pain, or facilitates joint motion prior to exercises. However, there is still limited evidence on the efficacy of electrical stimulation and thus any conclusions drawn about this method remain controversial. Recently, Microcurrent Electrical Neuromuscular Stimulation (MENS) has received significant attention as a potential method of electrical stimulation. In this study, we investigated the effect of microcurrent treatment in rheumatoid arthritis rat. Methods: Subjects were allocated either to the control group or experimental group, which was subject to microcurrent stimulation. Interleukin-1 expression in the metatarsophlangeal joint and the oedema index in the ankle were used for classification and subsequent evaluation of pathology. Subjects were assessed at 1, 7 and 14 days after inducing rheumatoid arthritis through adjuvant injection. Thirty-six subjects, 18 in each group, were used in this study. Statistical analysis was performed by calculating the differences between the two groups and between each interval assessment. Categorical variables were compared between the two groups with the paired-T test. The one-way ANOVA test was performed to assess changes in ordinal variables. Results: Baseline characteristics were similar in both groups. Statistically significant differences were found between the two groups. The biological marker of pro-inflammatory cytokine and oedema index were decreased in response to this treatment. Conclusion: These data show that treatment of rheumatoid arthritis with a microcurrent stimulation device reduced the oedema index and pro-inflammatory cytokine IL-1.

• 한국신재생에너지학회:학술대회논문집
• /
• 한국신재생에너지학회 2007년도 추계학술대회 논문집
• /
• pp.453-456
• /
• 2007

감압 증류 후 생성되는 중질유의 고도화를 위하여 코킹 공정을 거친 후 정유 부산물로 생성되는 열적으로 매우 안정하고, 높은 발열량을 갖는 반면 황, 바나듐 함량이 높은 석유코크스의 효과적인 이용을 위하여 본 연구에서는 가스화 공정을 적용하였다. 1T/D 용량의 분류층 가스화기를 이용하여 유연탄(drayton coal), 석유코크스, 또는 혼합한 경우의 가스화 성능을 알아보았으며, 각각의 경우에 대하여 비교하여 보았다. 높은 열 안정성을 갖는 석유코크스의 효과적인 가스화를 위하여 반응기 내 체류시간 및 버너 노즐 변경에 따른 가스화 성능 개선을 시도하였으며, 이때의 온도, 산소/원료 공급량 조건에 따른 생성가스 성분 및 탄소전환율, 냉가스효율 변화 특성을 알아보았다. 버너 노즐 구경 변경으로 인한 슬러리의 미립화를 통하여 향상된 탄소전환율 및 냉가스효율을 얻을 수 있었다.

• 대한전기학회:학술대회논문집
• /
• 대한전기학회 2001년도 하계학술대회 논문집 A
• /
• pp.261-263
• /
• 2001

오늘날 전력계통에서 개폐기, 차단기들은 케이블 충전이나 선로충전, 콘덴서 뱅크의 부하전류와 같은 진상 전류의 스위칭을 많이 하게 된다. 이때 진상 전류의 크기는 개폐기나 차단기의 정격 차단전류보다 그 크기가 매우 작다. 그러나 차단 책무는 개폐기나 차단기에 상당히 가혹하며, 이는 차단 후 극간에 걸리는 과도한 회복전압에 기인한다[2,3]. 상용주파 회복전압은 차단 성능을 검증하는 요소중의 하나로서 사고시 임피던스에 의해 변화한다. 본 논문에서는 IEC 60265-1에 따른 케이블 충전 전류 시험(Test duty 4a) 회로를 모의하고 IEC 60265-1에서 규정하는 규정치 이내에서 영상분 임피던스의 변화에 따른 상용주파 회복전압의 변화를 살펴보았다[1].

• IMMUNE NETWORK
• /
• 제3권2호
• /
• pp.136-144
• /
• 2003

Oral administration of antigen has long been considered as a promising alternative for the treatment of chronic autoimmune diseases including rheumatoid arthritis (RA), and oral application of type II collagen (CII) has been proven to improve pathogenic symptoms in RA patients without problematic side effects. To further current understandings about the immune suppression mechanisms mediated by orally administered antigens, we examined the changes in IgG subtypes, T-cell proliferative response, and proportion of interleukin (IL)-10 producing Th subsets in a time course study of collagen induced arthritis (CIA) animal models. We found that joint inflammation in CIA mouse peaked at 5 weeks after first immunization with CII, which was significantly subdued in mice pre-treated by repeated oral administration of CII. Orally tolerized mice also showed increase in their serum level of IgG1, while the level of IgG2a was decreased. T-cell proliferation upon CII stimulation was also suppressed in lymph nodes of mice given oral administration of CII compared to non-tolerized controls. When cultured in vitro in the presence of CII, T-cells isolated from orally tolerized mice presented higher proportion of $CD4^+IL-10^+$ subsets compared to non-tolerized controls. Interestingly, such increase in IL-10 producing cells were obvious first in Peyer's patch, then by 5 weeks after immunization, in mesenteric lymph node and spleen instead. This result indicates that a particular subset of T-cells with immune suppressive functions might have migrated from the original contact site with CII to inflamed joints via peripheral blood after 5 weeks post immunization.