• Title/Summary/Keyword: Tumor necrosis factor-$\alpha$ ($TNF-{\alpha}$)

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Changes of Plasma Tumor Necrosis Factor α and C-Reactive Protein Levels in Patients with Hypertension Accompanied by Impaired Glucose Tolerance and their Clinical Significance

  • Xiao, Qiang;Wang, Lan-Ping;Ran, Zhang-Shen;Zhang, Xin-Huan
    • Asian Pacific Journal of Cancer Prevention
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    • v.16 no.8
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    • pp.3389-3393
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    • 2015
  • Background: Chronic inflammation could affect the occurrence and development of malignant tumors. To explore the levels of tumor necrosis factor ${\alpha}$ (TNF-${\alpha}$) and C-reactive protein (CRP) in patients accompanied by impaired glucose tolerance (IGT) and their clinical significance. Materials and Methods: A total of 210 patients hospitalized in Affiliated Hospital of Taishan Medical University from Jun., 2013 to Dec., 2014 were selected, in which 92 cases were accompanied by IGT. Meanwhile, 80 randomly-selected healthy people by physical examination were as the control. The levels of routine biochemical indexes, plasma TNF-${\alpha}$ and CRP in all subjects were measured. Results: Both systolic and diastolic pressures in hypertension group and hypertension plus IGT group were significantly higher than in control group (p<0.01), but there was no statistical significance between these two groups (p>0.05). The levels of fasting plasma glucose (FPG) and blood glucose 2 h after taking glucose in hypertension plus IGT group were markedly higher than other groups (p<0.01). Homeostasis model assessment-insulin resistance (HOMA-IR), TNF-${\alpha}$ and CRP contents were on the progressive increase in control, hypertension and hypertension plus IGT groups, but significant differences were presented among each group (P<0.01). Hypertension accompanied by IGT had a significantly-positive association with CRP, TNF-${\alpha}$, FPG and blood glucose 2h after taking glucose. Conclusions: The levels of plasma TNF-${\alpha}$ and CPR in patients with hypertension accompanied by IGT increase significantly, indicating that inflammatory reaction in these patient increases, thus suggesting that these patients should be focused regarding cancer prevention.

The Effect of Korean Mistletoe Extract M11C (Non-Lectin Components) on the Tumor Necrosis $Factor-{\alpha}$ Secretion from Mouse Splenic Macrophages and on the Inhibition of Sarcoma 180-Induced Tumor Growth in Mice (한국산 겨우살이 추출물 M11C(비렉틴 구성물질)의 생쥐 비장 대식세포로부터 Tumor Necrosis $Factor-{\alpha}$ 분비효과와 생쥐에 Sarcoma 180으로 유도된 육종암의 성장 억제효과)

  • Sung, Ki-Tai;Kang, Tae-Bong;Jun, Myung-Ha;Chang, Sung-Ho;Lee, Jun-Ho;Kim, Jong-Bae;Choi, Wahn-Soo;Yoo, Yung-Choon;Seong, Nak-Sul;Lee, Sung-Tae;Sung, Hyun-Jea;Her, Erk
    • Korean Journal of Pharmacognosy
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    • v.34 no.3 s.134
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    • pp.210-217
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    • 2003
  • Korean mistletoe (Viscum album) extract has been found to posses immunostimulatory activity. In this study, Korean mistletoe extract, M11C (non-lectin components), was used to know whether this extract might activate mouse splenic macrophages to produce tumor necrosis $factor-{\alpha}\;(TNF-{\alpha}$) and might play a role in anticancer. To know the effect of M11C on the production of $TNF-{\alpha}$, the splenic macrophages were treated by the M11C, and then collected the supernatant (M11C stimulated splenic macrophage-conditioned media; MSCM). MSCM was analyzed for the $TNF-{\alpha}$ secretion by means of ELISA and immunoblotting, and mRNA expression was analyzed by RT-PCR. The S-180 murine sarcoma model was established to know the effect of M11C on the inhibition of tumor growth. M11C had the effect of $TNF-{\alpha}$ production from splenic macrophages performed by ELISA technique. This ELISA data was reconfirmed by immunoblotting assay. The effects of M11C on the expression of $TNF-{\alpha}$ mRNA from the macrophages was also shown. M11C also had the inhibitory effect of S-180 tumor growth. These data suggest that Korean mistletoe extract M11C may be used for an immunomodulator.

Nitric Oxide, TNF-${\alpha}$ and TGF-${\beta}$ Formation of Rat Kupffer Cell Activated by the ${\beta}$-Glucan from Ganoderma lucidum (영지의 ${\beta}$-glucan성 다당류에 의해 활성화된 흰쥐 간내 Kupffer 세포의 NO, TNF-${\alpha}$ 및 TGF-${\beta}$ 형성)

  • Han, Man-Deuk;Lee, June-Woo;Jeong, Hoon;Kim, Yong-Seok;Ra, Su-Jung;Yoon, Kyung-Ha
    • Microbiology and Biotechnology Letters
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    • v.27 no.1
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    • pp.28-34
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    • 1999
  • Ganoderan (GAN), an immunomodulating ${\beta}$-glucan from mushroom Ganoderma lucidum, was evaluated for its ability to induce formation of nitric oxide (NO), tumor necrosis factor-${\alpha}$(TNF-${\alpha}$) and transforming growth factor (TGF-${\beta}$) from rat Kupffer cell in vitro. Hepatic macrophages activated by GAN significantly elevated concentration of NO and TNF-${\alpha}$ in cultured medium, but not significantly elevated that of TGF-${\beta}$. GAN-activated Kupffer cells secrete 14.9${\mu}$M (p<0.01) of NO and 2619.5${\rho}$g/ml (p<0.01) of TNF-${\alpha}$after 36hr of incubation at 37$^{\circ}C$. The results revealed that GAN enhanced 4-fold production of NO and 19 fold formation of TNF-${\alpha}$ compared to the control. The proliferation of GAN-activated Kupffer cells was inhibited as compared with its negative control. Comparing the activity among glucans derived from microorganisms, highly branched zymosan, glucomannan from Saccharomyces cerevisiae, significantly increased TNF-${\alpha}$ and NO production. These results indicate that the ${\beta}$-glucan from G. lucidum activates rat Kupffer cell and secretes NO and TNF-${\alpha}$. It also suggest that rat Kupffer cell posses certain receptor for ${\beta}$-anomeric glucan.

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Anti-inflammatory Effects of Saussurea Lappa Extracts in Murine Macrophages (설치류 대식세포에서 목향(木香) 추출물의 항염증 효과)

  • Lee, Min-Suk;Ryu, Do-Gon;Kwon, Kang-Beom
    • Journal of Physiology & Pathology in Korean Medicine
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    • v.25 no.2
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    • pp.275-279
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    • 2011
  • In order to validate the use of Saussurea Lappa as an anti-inflammatory drug in the traditional Korean medicine, I have investigated the effects of water-soluble extract of Saussurea Lappa (ESL) on the production of pro-inflammatory tumor necrosis factor-alpha (TNF-${\alpha}$) in murine RAW 264.7 macrophages stimulated with the endotoxin lipopolysaccharide (LPS). The extract inhibited dose-dependently TNF-${\alpha}$ production without its cytotoxic effect on the macrophages, as measured by enzyme-linked immunosorbent assay, and significantly decreased mRNA levels of TNF-${\alpha}$, as determined using reverse transcription polymerase chain reaction. The extract also inhibited LPS-induced activation of nuclear factor-${\kappa}B$, thereby resulting in TNF-${\alpha}$ gene expression. These results suggest that ESL may have therapeutic potential in the control of inflammatory diseases mediated by activated macrophages.

Inhibitory Principles from Magnolia officinalis on Tumor Necrosis $Factor-{\alpha}$ Production in Lipopolysaccharide-Activated RAW264.7 cells

  • Cho, Jae-Youl;Park, Ji-Soo;Chae, Sook-Hee;Lee, June-Goo;Yoo, Eun-Sook;Baik, Kyong-Up;Lee, Jong-Soo;Park, Myung-Hwan
    • Natural Product Sciences
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    • v.5 no.2
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    • pp.70-74
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    • 1999
  • In the course of a search for tumor necrosis factor $(TNF)-{\alpha}$ inhibitory compounds from medicinal plants, we identified neolignans, honokiol and magnolol, from the alcoholic extract of Magnolia offcinalis as active inhibitory principles. These compounds dose-dependently inhibited $TNF-{\alpha}$ production without displaying cytotoxicity and their inhibitory activities measured by $IC_{50}$ values were 53.7 and $61.4\;{\mu}M$, respectively.

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Effect of Chong-Myung-Tang on the Production of Tumor Necrosis Factor a from Brain Astrocytes (뇌신경교(腦神經膠) 성장세포(星狀細胞)로부터 종양괴사인자 알파의 생성(生成)에 있어서 총명탕(聰明湯)의 효과(效果))

  • Lee Jong-Gil;Gang Hyeong-Won;Lyu Yeong-Su
    • Journal of Oriental Neuropsychiatry
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    • v.10 no.1
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    • pp.109-119
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    • 1999
  • We investigated whether an aqueous extract of Chong-Myung-Tang inhibits secretion of tumor necrosis $factor-{\alpha}$ $(TNF-{\alpha})$ from primary cultures of mouse astrocytes. Chong-Myung-Tang dosedependently inhibited the $TNF-{\alpha}$ secretion by astrocytes stimulated with substance P (SP) and lipopolysaccharide (LPS). Interleukin-1 (IL-1) has been shown to elevate $TNF-{\alpha}$ secretion from LPS-stimulated astrocytes while having no effect on astrocytes in the absence of LPS. We therefore investigated whether IL-1 mediated inhibition of $TNF-{\alpha}$ secretion from astrocytes by Chong-Myung-Tang. Treatment of Chong-Myung-Tang to astrocytes stimulated with both LPS and SP decreased IL-1 secretion. Moreover, incubation of astrocytes with IL-1 antibody abolished the synergistic cooperative effect of LPS and SP. These results suggest that Chong-Myung-Tang may inhibits $TNF-{\alpha}$ secretion by inhibiting IL-1 secretion and that Chong-Myung-Tang has a antiinflammatory activity in the central nervous system.

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Regulation of Tumor Necrosis Factor-${\alpha}$-induced Airway Mucin Production and Gene Expression by Carbenoxolone, Prunetin, and Silibinin

  • Lee, Hyun-Jae;Lee, Su-Yel;Jeon, Byeong-Kyou;Lee, Jae-Woo;Lee, Mi-Nam;Kim, Ju-Ock;Lee, Choong-Jae
    • Tuberculosis and Respiratory Diseases
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    • v.69 no.5
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    • pp.348-353
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    • 2010
  • Background: In this study, we tried to investigate whether carbenoxolone, prunetin, and silibinin affect tumor necrosis factor (TNF)-${\alpha}$-induced MUC5AC mucin production and gene expression from human airway epithelial cells. Methods: Confluent NCI-H292 cells were pretreated with each agent (carbenoxolone, prunetin, and silibinin) for 30 min and then stimulated with TNF-${\alpha}$ for 24 hours. The MUC5AC mucin gene expression and mucin protein production were measured by reverse transcription-polymerase chain reaction and enzyme linked immunosorbent assay, respectively. Results: Carbenoxolone, prunetin and silibinin inhibited the production of MUC5AC mucin protein induced by TNF-${\alpha}$; the 3 compounds also inhibited the expression of MUC5AC mucin gene induced by TNF-${\alpha}$. Conclusion: This result suggests that carbenoxolone, prunetin and silibinin can inhibit mucin gene expression and production of mucin protein induced by TNF-${\alpha}$, by directly acting on airway epithelial cells.

Effect of TNF-$\alpha$ Gene Transfer to Respiratory Cancer Cell Lines on Sensitivity to Anticancer drugs (호흡기계암세포주에서 TNF-$\alpha$ 유전자의 이입이 항암제 감수성에 미치는 효과)

  • Mo, Eun-Kyung;Lee, Jae-Ho;Lee, Kye-Young;Yoo, Chul-Gyu;Kim, Young-Whan;Han, Sung-Koo;Shim, Young-Soo;Choi, Hyung-Seok
    • Tuberculosis and Respiratory Diseases
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    • v.42 no.3
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    • pp.302-313
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    • 1995
  • Background: Tumor necrosis factor(TNF) showed antitumor cytolytic effects on sensitive tumor cells in numerous in vivo and in vitro studies. But it could not be administered systemically to human because of severe systemic adverse effects at effective concentrations against tumor cells. Many studies showed that a high concentrations of TNF in the local milieu may evoke in vivo TNF-responsive mechanisms sufficient to suppress tumor growth. Recently developed technique of TNF gene transfer to tumor cells using retrovirus vector could be a good candidate for local TNF administration. TNF is also known to synergistically enhance in vitro cytotoxicity of chemotherapeutic drugs targeted to DNA topoisomerase II against TNF-sensitive tumor cell lines. In this study the in vitro chemosensitivity against DNA topoisomerase II targeted chemotherapeutic drugs was evaluated using some respiratory cancer cell lines to which TNF gene had been transferred. Method: NCI-H2058, a human mesothelioma cell line, A549, a human lung adenocarcinoma cell line and WEHI 164 cell line, a murine fibrosarcoma cell line were treated with etoposide and doxorubicin, which are typical topoisomerase II - targeted chemotherapeutic agents, at different concentration. The resultant cytotoxicity was measured by MIT assay. Then the cytotoxicity of the same chemotherapeutic agents was measured after TNF-$\alpha$ gene-transfer and the two results were compared. Results: The cytotoxicity was not increased significantly in WEHI164 cell line and A549 cell line but statistically significant increase was observed in H2058 cell line when TNF-$\alpha$ gene was transferred(p<0.05). Conclusion: These findings show that TNF-$\alpha$ gene transfer to respiratory cancer cell lines results in variable effects on chemosensitivity against topoisomerase II inhibitor among different cell lines in vitro and can be additively cytotoxic in certain selective tumor cell lines.

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Effects of dietary acetaminophen and vitamin C supplement on serum cortisol and tumor necrosis factor-alpha concentrations in pigs vaccinated with foot-and-mouth disease vaccine

  • Cha, Chun-Nam;Lee, Beom-Jun;Park, Eun-Kee;Yoo, Chang-Yeol;Kim, Suk;Lee, Hu-Jang
    • Korean Journal of Veterinary Research
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    • v.57 no.3
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    • pp.197-200
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    • 2017
  • This study evaluated the effect of a combination of acetaminophen and vitamin C (CAV) on reducing serum cortisol and tumor necrosis $factor-{\alpha}$ ($TNF-{\alpha}$) concentrations in piglets vaccinated with foot-and-mouth disease (FMD) vaccine. Piglets were vaccinated with FMD vaccine and treated with CAV at concentrations of 0.0, 0.5, 1.0, and 2.0 kg/ton feed (P-CON, AD-1, AD-2, and AD-3, groups, respectively) for 5 days post-vaccination. Cortisol and $TNF-{\alpha}$ levels at 5 days post-treatment in the AD-1-3 groups were significantly lower than that in the P-CON group (p < 0.05). There were no significant differences between AD-2 and AD-3 groups and non-vaccinated, non-CAV-treated piglets.

Association between Tumor Necrosis Factor-$\alpha$ Gene Polymorphism and Bronchopulmonary Dysplasia in Preterm Infants (조산아 기관지폐이형성증과 Tumor Necrosis Factor-$\alpha$ 유전자 다형성과의 연관성)

  • Jo, Heui-Seung;Chang, Yoon-Hwan;Kim, Han-Suk;Kim, Byeong-Il;Choi, Jung-Hwan
    • Neonatal Medicine
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    • v.18 no.1
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    • pp.42-48
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    • 2011
  • Purpose: Several factors including prolonged inflammatory response are thought to contribute to the pathogenesis of bronchopulmonary dysplasia (BPD). The clinical findings can be explained by an increased production of proinflammatory cytokines such as tumor necrosis factor alpha (TNF-$\alpha$ ). We investigated the relationship between susceptibility to BPD and TNF-$\alpha$ promoter polymorphisms to identify genetic factors of the disease. Methods: Thirty-eight preterm infants who had developed BPD and 55 controlled infants with a birth weight <1,500 g were analyzed for TNF-$\alpha$ genotypes. The alleles of five promoter sites (-1031/-863/-857/-308/-238) of TNF-$\alpha$ gene were determined using $Taqman^{(R)}$-based allelic discrimination assays. Results: Gestational age ($27^{+5}{\pm}2^{+0}$ wk vs. $29^{+2}{\pm}1^{+4}$ wk, P<0.0001) and birth weight (990${\pm}$270 g vs. 1,220${\pm}$230 g, P<0.0001) were lower in the BPD group compared to the control group. The incidence of respiratory distress syndrome (71.1% vs. 49.1%, P=0.035) and patent ductus arteriosus (71.1% vs. 50.9%, P=0.052) was higher in the BPD group compared to the control group. The frequencies of the alleles and genotypes of five promoter sites (-1031/-863/-857/-308/-238) of TNF-$\alpha$ gene did not show differences between the BPD group and the control group. Conclusion: TNF-$\alpha$ promoter polymorphisms are not associated with susceptibility to BPD in Korean preterm infants.