• Food Science and Preservation
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• v.23 no.3
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• pp.378-386
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• 2016

Anti-atherogenic effects in tumor necrosis factor-${\alpha}$ (TNF-${\alpha}$)-stimulated human umbilical vein endothelial cells (HUVEC) are involved in the suppression of oxidative stress, cell adhesion molecules, and pro-inflammatory factors. This study investigated the vascular inflammation inhibitory activity of traditional Doenjang plays a key role in the pathogenesis and progression of atherosclerosis. The protective effects of Korean Deonjang was investigated on the expression of cell adhesion molecules (CAMs) in tumor necrosis factor (TNF)-${\alpha}$-induced human umbilical vascular endothelial cells (HUVECs). Deonjang extracts (20, 50, $100{\mu}g/mL$) decreased the expression of 20 ng/mL TNF-${\alpha}$-induced vascular cell adhesion molecule (VCAM)-1 intracellular adhesion molecule (ICAM)-1 proteins, and their corresponding mRNA levels. Nitric oxides (NO) produced by endothlial nitric oxides synthase (eNOS) dilated blood vessels, which had protective effects against platelet and leukocyte adhesion. While TNF-${\alpha}$-induced suppressed the production of nitric oxide in HUVECs, Doenjang restored NO production in HUVECs. In addition, Deonjang reduced the TNF-${\alpha}$-induced expression of inducible NO synthase (iNOS) and cyclooxygenase (COX)-2 mRNA levels. These results suggested that Doenjang can inhibited the production of cell adhesion molecules and inflammatory mediators, which could be a potential candidate for preventing atherosclerosis.

• The Korean Journal of Physiology and Pharmacology
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• v.1 no.5
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• pp.515-521
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• 1997

Endothelial cells play a central role in the inflammatory processes, and activation of nuclear factor kappa B ($NF-_{\kappa}B$) is a key component in that inflammatory processes. Previously, we reported that tumor necrosis factor alpha($TNF{\alpha}$) had protective effect of cell death induced by serum deprivation and this protection was related to $NF-_{\kappa}B$ activation. Inducible nitric oxide synthase (iNOS) is a member of the molecules which transcription is regulated mainly by $NF-_{\kappa}B$. And the role of nitric oxide (NO) generated by iNOS on cell viability is still controversial. To elucidate the mechanism of $TNF{\alpha}$ and $NF-_{\kappa}B$ activation on cell death protection, we investigate the effect of NO on the cell death induced by serum- deprivation in bovine cerebral endothelial cells in this study. Addition of $TNF{\alpha}$, which are inducer of iNOS, prevented serum-deprivation induced cell death. Increased expression of iNOS was confirmed indirectly by nitrite measurement. When selective iNOS inhibitors were treated, the protective effect of $TNF{\alpha}$ on cell death was partially blocked, suggesting that iNOS expression was involved in controlling cell death. Exogenously added NO substrate (L-arginine) and NO donors (sodium nitroprusside and S-nitroso-N-acetylpenicillamine) also inhibited the cell death induced by serum deprivation. These results suggest that NO has protective effect on bovine cerebral endothelial cell death induced by serum-deprivation and that iNOS is one of the possible target molecules by which $NF-_{\kappa}B$ exerts its cytoprotective effect.

• Journal of Acupuncture Research
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• v.24 no.3
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• pp.197-205
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• 2007

Objectives : Tumor necrosis factor-${\alpha}$(TNF ${\alpha}$) is a proinflammatory cytokine involved in the pathogenesis of rheumatoid arthritis. This study was designed to investigate the relation between TNF-${\alpha}$ gene polymorphism and rheumatoid arthritis in Korean population. Methods : This study was carried out on 103 rheumatoid arthritis patients who fulfilled the American College of Rheumatology 1987 revised criteria for rheumatoid arthritis and 208 healthy control subjects. Blood samples from all subjects were obtained for DNA extraction. The extracted DNA was amplified by polymerse chain reaction(PCR). PCR products were visualized by 2% agarose gel electrophoresis. We investigated the genotyping of TNF-${\alpha}$ by using Pyrosequencing. Results: The genotypes of TNF-${\alpha}$ gene were GG, AG and AA. While the distribution of TNF-${\alpha}$ polymorphism in control subjects was 92.31%, 7.21%, 0.48% respectively, in rheumatoid arthritis patients was 93.20%, 6.80%, 0.00%(GG, AG, AA). There was no statistical significant allelic frequency difference between control and rheumatoid arthritis groups. Conclusions : We concluded that there was no significant association between TNF-${\alpha}$ gene polymorphism and rheumatoid arthritis. However, the findings of this study need to be confirmed in more patients and further studies.

• Pediatric Gastroenterology, Hepatology & Nutrition
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• v.15 no.1
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• pp.44-51
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• 2012

Purpose: Tumor necrosis factor-${\alpha}$ (TNF-${\alpha}$) polymorphism has been suggested to play an important role in the pathogenesis of non-alcoholic fatty liver disease (NAFLD) in obese adults, and known to be a mediator of insulin resistance. In this study, we evaluated the role of TNF-${\alpha}$ promoter polymorphisms and insulin resistance in the development of NAFLD in obese children. Methods: A total of 111 obese children (M:F=74:37; mean age, $11.1{\pm}2.0$ yrs) were included. The children were divided into 3 groups: controls (group I, n=61), children with simple steatosis (group II, n=17), and children with non-alcoholic steatohepatitis (group III, n=33). Serum TNF-${\alpha}$ levels, homeostasis model assessment of insulin resistance (HOMA-IR), and TNF-${\alpha}$ -308 and -238 polymorphisms were evaluated. Results: There were no differences in TNF-${\alpha}$ polymorphism at the -308 or the -238 loci between group I and group II + III ($p$=0.134 and $p$=0.133). The medians of HOMA-IR were significantly different between group I and group II + III ($p$=0.001), with significant difference between group II and group III ($p$=0.007). No difference was observed in the HOMA-IR among the genotypes at the -308 locus ($p$=0.061) or the -238 locus ($p$=0.207) in obese children. Conclusion: TNF-${\alpha}$ promoter polymorphisms at the -308 and -238 loci were not significantly associated with the development of NAFLD in children; nevertheless, insulin resistance remains a likely essential factor in the pathogenesis of NAFLD in obese children, especially in the progression to NASH.

• Journal of Convergence for Information Technology
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• v.9 no.6
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• pp.218-226
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• 2019

In this study, we investigated the possibility of Kaempferia Galanga(KG) hot water extract on the antioxidant, cytotoxic and anti-inflammatory efficacy as a cosmetic ingredient. Antioxidant effects were evaluated based on DPPH and ABTS radical scavenging activity, FRAP assay, and total polyphenol contents. The MTT assay was used to confirm the cell toxicity in mouse macrophage RAW264.7 cells. Anti-inflammatory effects were also investigated in LPS-induced RAW264.7 cells by measuring secretion of NO, $TNF-{\alpha}$ and iNOS, $TNF-{\alpha}$ mRNA expression level. As a result, DPPH and ABTS radical scavenging activities were increased in a concentration-dependent manner. The ferric reducing antioxidant power(FRAP) was the highest at 5 mg/mL as 24.5 uM. The measurements of total polyphenol content was $1.28{\pm}0.064mg\;GAE/g$. The cytotoxicity of the KG extract results showed no cytotoxicity at concentration of 0.625 to 2.5 mg/mL. In addition, the extract of KG significantly suppressed the LPS-induced nitrite, $TNF-{\alpha}$ secretion and the mRNA expression of iNOS, $TNF-{\alpha}$ in RAW264.7 cells. Taken together, these data suggest that the KG hot water extracts can be used as a safe and functional cosmetic raw material.

• Herbal Formula Science
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• v.16 no.2
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• pp.101-114
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• 2008

Objective : The purpose of this study was to investigate the anti-inflammatory effects of Hwagae-san extract(HGSE) on the peritoneal macrophage. Methods : To evaluate anti-inflammatory effects of HGSE, We measured cytokines(interleukin-6; IL-6, interleukin-12; IL-12, tumor necrosis factor-${\alpha}$; TNF-${\alpha}$) and nitric oxide(NO) production in lipopolysaccharide(LPS)-induced macrophages. Furthermore, We examined molecular mechanism using western blot and also LPS-induced endotoxin shock. Results : 1. HGSE did not have any cytotoxic effect in the peritoneal macrophages. 2. HGSE reduced LPS-induced IL-6, TNF-${\alpha}$, IL-12 and NO production in peritoneal macrophages. 3. HGSE inhibited the activation of extracelluar signal-regulated kinase(ERK), C-Jun NH2-terminal kinase(JNK) but not of p38, degradation of IkB-${\alpha}$ in the LPS-stimulated peritoneal macrophages. 4. HGSE inhibited the production of TNF-$\alpha$, IL-6 and IL-12 in serum after LPS injection. Conclusion : These results suggest that HGSE may inhibit the production of TNF-${\alpha}$, IL-6, and IL-12 through inhibition of ERK and JNK activation, and that HGSE may be beneficial for inflammatory diseases.

• Journal of Ginseng Research
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• v.33 no.1
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• pp.1-7
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• 2009

Clinical and animal studies have shown that free radical overload is an important cause for a variety of diseases. Although ginseng has been recognized as antioxidant, how it modulates anti-oxidative process at the molecular level remains unknown. Free radical production is induced by tumor necrosis factor-$\alpha$ (TNF-$\alpha$) under the stress condition, and (TNF-$\alpha$) release is activated by TNF-$\alpha$-converting enzyme (TACE). Since TACE inhibitor is also well known for anti-inflammatory agent, ginseng seems to show anti-oxidative activity by repressing TACE pathway. Further studies on signal transduction would be warranted to elucidate molecular action mechanisms of ginseng on anti-oxidation and anti-inflammation.

• Korean Journal of Food Science and Technology
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• v.45 no.3
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• pp.385-390
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• 2013

The effect of tuna extracts on the production of nitric oxide (NO) and cytokines including interleukin-6 (IL-6), tumor necrosis factor-${\alpha}$ (TNF-${\alpha}$), and interferon-${\gamma}$ (IFN-${\gamma}$), was investigated. All extracts and fractions from tuna significantly reduced NO production induced by lipopolysaccharide (LPS). The acetone+methylene chloride (A+M) extract, n-hexane and 85% aqueous methanol (MeOH) fractions had stronger inhibitory effects among them. The 85% aqueous MeOH fraction at a 10-${\mu}g$ concentration significantly decreased LPS-induced IL-6 and TNF-${\alpha}$ productions at 6 h of incubation. In the case of LPS-induced IFN-${\gamma}$ production, the 85% aqueous MeOH fraction at a 3-${\mu}g$ concentration showed significantly higher levels at 48 h of incubation. These results show that the 85% aqueous MeOH fraction inhibited the production of NO and pro-inflammatory cytokines (IL-6, TNF-${\alpha}$), suggesting that this fraction acts as a potent immunomodulator.

• Journal of Life Science
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• v.18 no.9
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• pp.1207-1211
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• 2008

The pro-inflammatory cytokine tumor necrosis factor-$\alpha$ (TNF-$\alpha$) is an important mediator of the immune response in hepatitis B virus (HBV) infection. Since the production of TNF-$\alpha$ is mostly regulated at the transcriptional level and polymorphisms in the TNF-$\alpha$ promoter alter its expression, TNF-$\alpha$ promoter polymorphisms could affect the pathogenesis of chronic HBV infection. In this study, we investigated the potential association of TNF-$\alpha$ promoter polymorphisms with chronic HBV infection. The study included 181 patients with chronic HBV infection, 201 persons who had been spontaneously recovered from hepatitis B, and 170 unrelated healthy controls. The -308G/A and -238G/A polymorphisms in the TNF-$\alpha$ promoter were analyzed by PCR-restriction fragment length polymorphism. The distribution of both the -308 and -238 genotypes in the patient group was not statistically different from that in the spontaneous recovery and control groups (p>0.05). There was also no significant difference in the allele frequency between the groups (p>0.05). The results suggest that the TNF-$\alpha$ -308 and -238 promoter polymorphisms are not associated with the development of chronic HBV infection in the Korean population.

• Journal of Pharmacopuncture
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• v.10 no.2 s.23
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• pp.73-79
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• 2007

Objectives : Tumor necrosis factor-${\alpha}{\cdot}$(TNF-${\alpha}{\cdot}$) is a proinflammatory cytokine involved in the pathogenesis of rheumatoid arthritis. This study was designed to investigate the relation between TNF-${\alpha}{\cdot}$ gene polymorphism and rheumatoid arthritis in Korean population. Methods : This study was carried out on 103 rheumatoid arthritis patients who fulfilled the American College of Rheumatology 1987 revised criteria for rheumatoid arthritis and 208 healthy control subjects. Blood samples from all subjects were obtained for DNA extraction. The extracted DNA was amplified by polymerse chain reaction(PCR). PCR products were visualized by 2% agarose gel electrophoresis. We investigated the genotyping of TNF-${\alpha}{\cdot}$ by using Pyrosequencing. Results : The genotypes of TNF-${\alpha}{\cdot}$ gene were GG, AG and AA. While the distribution of TNF-${\alpha}{\cdot}$ polymorphism in control subjects was 92.31%, 7.21%, 0.48% respectively, in rheumatoid arthritis patients was 93.20%, 6.80%, 0.00%(GG, AG. AA). There was no statistical significant allelic frequency difference between control and rheumatoid arthritis groups. Conclusion : We concluded that there was no significant association between TNF-${\alpha}{\cdot}$ gene polymorphism and rheumatoid arthritis. However, the findings of this study need to be confirmed in more patients and further studies.