자궁내막증의 존재유무에 따른 혈장과 복강액내의 TNF - α 농도 ; TNF - α 가 자궁내막증의 병인인가 ?

김호성(Ho Sung Kim),이수미(Soo Mi Lee),신희경(Hee Gung Shin),문혜경(Hye Kyoung Mun),조태일(Tae Il Cho),강정배(Jeong Bae Kang),이영경(Young Kyeong Lee) 대한산부인과학회 2001 Obstetrics & Gynecology Science Vol.44 No.9

N/A Objective : Our purpose of study was to investigate whether in vivo levels of tumor necrosis factor-α in plasma and peritoneal fluid (PF) differ in women with and without endometriosis. Design : Prospective and case-control study. Methods : Fifty-seven women with laparotomy or laparoscopic findings of minimal to severe endometriosis, and forty-two women with no visual evidence of pelvic endometriosis and with benign gynecologic disease. Tumor necrosis factor-α levels in plasma and PF were determined using commercial ELISA. Tumor necrosis factor-α concentrations were compared among women with and without endometriosis, and then also were compared according to the revised American Fertility Society classification. Results : Tumor necrosis factor-α concentrations were not significantly increased in the plasma and PF of women with endometriosis than in matched normal controls. Tumor necrosis factor-α concentrations in endometriosis stage III and IV were sightly increased, which were not increased statistically significant. Conclusions : Plasma and PF tumor necrosis factor-α levels were not different between women with and without endometriosis. Our results do not rule out the hypothesis that tumor necrosis factor-α may be involved in the pathogenesis of some features of endometriosis.

종양괴사인자-α로 유발시킨 삼출성 중이염에서 TNF Soluble Receptor TypeⅠ의 역할

이동희,박용수,최영철,전은주,여상원 대한이비인후과학회 2000 대한이비인후과학회지 두경부외과학 Vol.43 No.9

난포액내에 존재하는 TNF - α 와 NO 의 농도가 난자의 질에 미치는 영향에 관한 연구

이규섭 ( K . S . Lee ) 대한산부인과학회 2001 Obstetrics & Gynecology Science Vol.44 No.7

N/A Objective: Our objective was to explain a relationship between concentrations of tumor necrosis factor- α (TNF- α) and nitric oxide (NO) in follicular fluid, oocyte quality, and outcomes of in vitro fertilization- embryo transfer 0VF-ET). Method: The concentrations of TNF- α and NO were measured in 115 follicular fluid samples collected from 43 patients undergoing IVF-ET program, due to tubal obstruction, some with endometriosis (8 patients) or hydrosalpinx (5 patients). A correlation of these factors concentrations and the oocyte quality, the oocyte marurity, and infertility associated disease was analyzed Result: No correlation was found between concentrations of NO and TNF- α in follicular fluid. NO concentrations in follicular fluids were significantly higher in patients with endometriosis (P<0.001) or hydrosalpinx (P<0.01) compared to the patients with just tubal obstruction. Follicular NO concentration differences according to oocyte maturity and oocyte quality were not found. In contrast, TNF- α concentrations in follicular fluids were significantly higher in poor quality oocytes (P<0.05) but were not associated with infertility-associated diseases, such as hydrosalpinx or endometriosis, and the oocyte maturity. No significant differences in follicular levels of NO and TNF- α as well as IVF-ET parameters of pregnant and nonpregnant groups were revealed. Conclusions: There is no significant correlation between the concentrations of NO and TNF- α in follicular fluid. NO levels in follicular fluid are altered in infertility-associated disease. However, TNF- α levels but not NO levels influence oocyte quality. These results suggest that the production of NO and TNF- α in follicular fluid may be regulated via different pathways and can be tempered with infertility-associated disease, thereby influencing oocyte quality locally.

실험동물에서 Lipopolysaccharide와 Thalidomide에 의한 Vascular Endothelial Growth Factor와 Tumor Necrosis Factor-α 발현의 변화

최동락,조창호,정진숙,홍숙희,윤길숙 대한대장항문학회 2004 Annals of Coloproctolgy Vol.20 No.3

Trans-10, cis-12 Conjugated Linoleic Acid Modulates Tumor Necrosis Factor-α Production and Nuclear Factor-κB Activation in RAW 264.7 Macrophages Through Formation of Reactive Oxygen Species

박소영,강병택,강지훈,양만표 한국임상수의학회 2014 한국임상수의학회지 Vol.31 No.6

The aims of this study were to explore the effects of conjugated linoleic acid (CLA) on reactive oxygenspecies (ROS) production in lipopolysaccharide (LPS)-naïve and LPS-stimulated RAW 264.7 macrophages and toexamine whether these effects affect the regulation of tumor necrosis factor-alpha (TNF-α) production, and nuclearfactor-kappa B (NF-κB) and peroxisome proliferator-activated receptor gamma (PPARγ) activation. Trans-10, cis-12(t10c12)-CLA increased the production of ROS, as well as TNF-α in LPS-naïve RAW 264.7 cells. The CLA-inducedTNF-α production was suppressed by treatment of diphenyleneiodonium chloride (DPI), a NADPH oxidase inhibitor. In addition, CLA enhanced the activities of NF-κB and PPARγ in LPS-naïve RAW 264.7 cells, and this effect wasabolished with DPI treatment. LPS treatment increased ROS production, whereas CLA reduced LPS-induced ROSproduction. LPS increased both TNF-α production and NF-κB activity, whereas t10c12-CLA reduced TNF-α productionand NF-κB activity in LPS-stimulated RAW 264.7 cells. DPI treatment suppressed LPS-induced ROS production andNF-κB activity. Moreover, DPI enhanced the inhibitory effects of t10c12-CLA on TNF-α production and NF-κBactivation in LPS-stimulated RAW 264.7 cells. However, neither t10c12-CLA nor DPI affected PPARγ activity in LPSstimulatedRAW 264.7 cells. Taken together, these data indicate that t10c12-CLA induces TNF-α production byincreasing ROS production in LPS-naïve RAW 264.7 cells, which is mediated by the enhancement of NF-κB activityvia PPARγ activation. By contrast, t10c12-CLA suppresses TNF-α production by inhibiting ROS production and NF-κB activation via a PPARγ-independent pathway in LPS-stimulated RAW 264.7 cells. These results suggest that t10c12-CLA can modulate TNF-α production and NF-κB activation through formation of ROS in RAW 264.7 macrophages

Peroxisome Proliferator-activated Receptor-γ가 단핵세포의 Tumor Necrosis Factor-α 생산에 미치는 영향

권은영,박철민,권재철,김시현,박선희,최수미,이동건,유진홍,최정현 대한감염학회 2010 Infection and Chemotherapy Vol.42 No.5

Background: We evaluated the effects of peroxisome proliferator-activated receptor-γ (PPAR-γ) on the production of tumor necrosis factor-α (TNF-α) and expression of nuclear factor-κB (NF-κB) in stimulated THP-1 cells, a human monocyte cell line. Materials and Methods: We evaluated the cytotoxic effect of 15-Deoxy-Δ12,14-prostaglandin J2 (15d-PGJ2), one of natural PPAR-γ ligands, using commercial cell proliferation assay. Cells were pretreated with 15d-PGJ2 and then stimulated with lipopolysaccharide (LPS) or lipoteichoic acid (LTA). The amount of TNF-α was measured by using commercial ELISA method. NF-κB activation was evaluated by Western blot analysis. Results: 15d-PGJ2 showed dose-dependent cytotoxic effect on the tested cells after 4 hr of treatment. Stimulation of cells by LPS or LTA induced TNF-αproduction. TNF-α production was markedly decreased in the cells pretreated with 15d-PGJ2compared to cells treated only with LPS or LTA in a dose-dependent manner. Pretreatment of 15d-PGJ2 reduced LPS or LTA induced NF-κB expression in the nuclear extracts of THP-1 cells. Conclusion: 15d-PGJ2 pretreatment decreased TNF-α production from the THP-1cells stimulated by LPS or LTA, and this assumed to be associated with inhibition of NF-κB activation.

건선 병변에서 Interleukin-8 과 Tumor necrosis factor - α 발현에 대한 면역조직화학적 연구

원덕환(Duck Hwan Won),김영근(Young Keun Kim),최광성(Gwang Sung Choi) 대한피부과학회 2001 大韓皮膚科學會誌 Vol.39 No.5

N/A Background: Psoriasis is a chronic skin disease characterized histologically by prominent keratinocyte hyperplasia and an early inflammatory cell infiltrate. However, the pathogenesis is not fully understood yet. Recently, there has been growing interest in the probable role of a T cell mediated immune response in the pathogenesis. Especially, cytokine network involved in psoriasis has been studied. Objective : This study was done to investigate the role of Interleukin-8(IL-8) and its inducer, Tumor necrosis factor-a(TNF-a) for pathogenesis of psoriasis. Methods: We performed immunohistochemical staining using antibodies for IL-8 and TNF- a in frozen skin samples of 14 psoriatic patients who had not been treated for psoriatic lesion for 1 month and 3 normal skin samples as controls. Results : There was no detectable discrete immunoreactivity for either TNF-a and IL-8 in epidermis and dermis of normal controls. In psoriatic lesions, the expression of TNF-a was found in dermal cells within the papillary dermis, particularly around blood vessels. The expression of IL-8 was presented on suprabasal keratinocytes above TNF- a-positive dermal tissue. Conclusion : Our results strongly suggest that histologic expression and functional interaction between IL-8 and its inducer, TNF- a have significant roles in the pathogenesis of psoriasis.

Expression of angiogenin, TGF-β, VEGF, APEX and TNF-α in oral squamous cell carcinoma

Ho-Sun Lee,Kyoung-Won Kim,Wun-Jae Kim 대한구강악안면외과학회 2006 대한구강악안면외과학회지 Vol.32 No.1

Purpose: The purpose of this study was to verify that the expressions of angiogenin, transforming growth factor-beta(TGF-β), vascular endothelial growth factor(VEGF), human apurinic/apyrimidinic endonuclease(APEX) and tumor necrosis factoralpha(TNF-α) were associated with the tumorigenesis of the oral squamous cell carcinoma(OSCC). Materials and Methods: Fifty-one samples of OSCC and fifteen normal oral mucosae were obtained to analyze the expression levels of above five factors. mRNA expressions were quantified by the quantitative competitive PCR(QC-PCR) method. After 2% agarose gel electrophoresis stained with ethidium bromide, the concentration of mRNA was calculated by a digital image analysis system. The expression levels of angiogenin, TGF-β, VEGF, APEX and TNF-αwere compared by unpaired Student’s ttests between cancer and normal tissues. We analyzed statistically to find the cut-off values that would be useful as diagnostic markers, and the linear regression analysis between every two factors of these five factors by SAS system. Results: All of these five factors (angiogenin: P<0.0037, TGF-β: P<0.0001, VEGF: P<0.0102, APEX: P<0.0023, TNF-α: P<0.0074) were significantly correlated with OSCC. In the analysis to find the cut-off values for the diagnosis, we could not find any value that had a reasonable sensitivity and specificity. In the linear regression analysis, there were correlations between angiogenin and TNF-α, TGF-βand VEGF, TGF-βand APEX, TGF-βand TNF-α, VEGF and APEX, VEGF and TNF-α, APEX and TNF-α. Conclusion: Our results suggest that not only angiogenin, TGF-β, VEGF, APEX and TNF-αare significantly associated with the tumorigenesis, but also the close relationship between these factors might enhance the tumorigenesis of OSCC. We can not find clinical availability for diagnosis.

Pertussis toxin-induced hyperacute autoimmune encephalomyelitis in Lewis rats is correlated with increased expression of inducible nitric oxide synthase and tumor necrosis factor alpha

Ahn, Meejung,Kang, Jongchul,Lee, Yongduk,Riu, Keyzung,Kim, Yong-sik,Jee, Youngheun,Matsumoto, Yoh,Shin, Taekyun 제주대학교 방사능이용연구소 2001 연구보고 Vol.15 No.-

자기면역성 뇌척수염(experimental autoimmune encephalomyelitis, EAE)은 뇌조직항원을 면역한 후 야기되는 염증성 질병으로 사람 다발성결화증의 한 모델로 연구되고 있다. 자기면역성 뇌염의 시작은 뇌조직항원에 반응하는 림프구가 중추신경계에 침윤되면서 마비를 나타내는데 이 과정 중에는 여러 종류의 pro-inflammatory mediator (tumor necrosis factor-alpha (TNF-α)와 inducible nitric oxide synthase (iNOS)등)가 관여하는 것으로 알려지고 있다. 이 연구에서는 염증의 진행 단계에 따라 염증 유도 또는 염증 억제의 상반된 기능을 갖는 것으로 알려진 TNF-α와 iNOS가 심급성 뇌척수염 진행에 어떠한 영향을 미치는지를 조사하였다. 뇌염을 유도하기 위한 항원으로는 랫트 척수 조직 유제를 complete Freund adjuvant와 혼합하여 뒷 발바닥에 주사하였으며 심한 뇌척수염을 유도하기 위하여 pertussis toxin(500ng/ea)을 면역하는 날 복강내로 주사하고 매일 체중과 마비 정도를 확인하였다. 독소를 주사한 실험군에서는 대조군(11일)에 비해 마비의 시작이 빨랐으며(9일), 대조군은 자연 회복하는 반면 독소룰 주사한 실험군에서는 모두 폐사하였다. 척수 조직 내 TNF-α 와 iNOS의 양적인 변화를 조사하기 위하여 Competitive PCR과 Western blot를 이용하였으며, 세포형을 구분하기 위하여 면역염색을 이용하였다. Competitive PCR결과 TNF-α는 PT를 투여한 자기면역성뇌척수염의 심한 마비기(EAE,G3)에서 PT를 투여하지 않은 대조군보다 약 5배가 증가하였으며(p<0.01), Western blot결과 iNOS는 PT를 투여한 군에서 정상조직에 비해 약 6배가 증가하였고, PT를 투여하지 않은 군에 비해서는 약 3개바 증가하였다(p<0.01). 면역염색결과 PT를 투여하지 않은 랫트보다 투여한 랫트의 척수조직에서 iNOS 양성 세포가 약 15배가 증가하였으며(p<0.01), 또한 연속절편에서 이들 세포가 큰포식세포임을 확인하였다. 이상의 결과를 종합해 볼 때, 자기면역성 뇌척수염의 초기 유도과정에서는 TNF-α와 iNOS는 염증의 약화에 관여됨을 알 수 있었다. The involvement of inducible nitric oxide synthase (iNOS) and tumor necrosis factor alpha (TNF-α), which have diverse roles in the progression of autoimmune disease models, was studied in pertussis toxin (PT-induced hyperacute experimental autoimmune encephalomyelitis (EAE) in Lewis rats. The expression of TNF-α mRNA(increased 5 fold, p<0.01) and iNOS protein (3 fold, p<0.01) was much greater in the spinal cords with PT(+) EAE at the peak stage of EAE than in those with PT(-) EAE, as shown by competitive PCR and Western blot analysis, respectively. Immunohistochemistry showed that the majority of EDI-positive macrophages in EAE lesions contained iNOS, and that three were many more iNOS-positive cells in the CNS lesions of PT(+) rats than in those of PT(-) rats. These findings suggest that PT-induced hyperacute EAE is partly mediated by the enhanced expression of iNOS and TNF-α in the early stages of rat EAE.

Effect of Conjugated Linoleic Acid on Nuclear Factor-κB Activation and Tumor Necrosis Factor-α Production in RAW 264.7 Cells Exposed to High Concentration of Glucose

이민지,강병택,강지훈,양만표 한국임상수의학회 2012 한국임상수의학회지 Vol.29 No.5

Diabetes-related complications in human and veterinary medicine have been shown to be associated with hyperglycemia-induced inflammation. It has been recently suggested that the onset of insulin resistance may be caused by over-production of inflammatory cytokines such as tumor necrosis factor (TNF)-α from immune cells. Conjugated linoleic acid (CLA) regulates inflammatory response through modulation of TNF-α expression. The objective of this study was to examine the effect of CLA on nuclear factor kappaB (NF-κB) p65 binding activity, inhibitory kappaB (IκB)-α expression, and TNF-α production from high glucose-treated RAW 264.7 cells. CLA was added to RAW cells that had been previously cultured with low or high concentration of glucose. The levels of TNF-α protein in the culture supernatant of RAW cells exposed to high concentrations of glucose were higher than those of cells exposed to low concentrations of glucose. The treatment with the high concentration of glucose in RAW cells increased levels of NF-κB p65 binding activity and the decreased IκB-α expression when compared with those of low glucose. The treatments in combination with CLA and glucose (low and high) glucose in RAW cells increased TNF-α production when compared with that glucose alone. These treatments with CLA increased TNF-α production in high glucosetreated RAW cells than those with low glucose. These treatments of CLA also showed higher NF-κB p65 binding activity and lower IκB-α expression in high glucose than those in low glucose condition. This suggests that CLA can increase NF-κB p65 binding activity and TNF-α production from high glucose-treated RAW 264.7 cells and is likely to promote hyperglycemia-induced inflammation.