• The Journal of Korean Medicine
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• v.26 no.1 s.61
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• pp.59-70
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• 2005

Objective: Tumor necrosis factor-a $(TNF-{\alpha})$, a potent immuno-modulator and pro-inflammatory cytokine, has been implicated in many pathological processes. In this study, the author examined whether promoter region polymorphism in the $TNF-{\alpha}$a gene at position-308 affect the odds of cerebral infarction (CI) and whether genetic risk is enhanced by sasang constitutional classification. Methods: 212 CI patients and 610 healthy controls were genotyped and determined according to sasang constitutional classification. The amplified genotypes were analyzed on $8\%$ polyacrylamide gel. The alleles were visualized by ethidium bromide staining. Primers for $TNF-{\alpha}$ were designed to incorporate a polymorphic site at a position -308 bp of the $TNF-{\alpha}$ gene into an NcoI restriction site. Restriction digests generated products of 87 and 20 bp for G allele and 107 bp for A allele. Results : A significant decrease was found for the $TNF-{\alpha}$ A allele in CI patients compared with controls (P=0.033, odds ratio, O.R.: 0.622). However, there was no significant association between $TNF-{\alpha}$ polymorphism and sasang constitution in CI patients. Conclusion: My finding suggests that $TNF-{\alpha}$promoter region polymorphism is responsible for susceptibility to CI in Koreans.

• Journal of Physiology & Pathology in Korean Medicine
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• v.21 no.4
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• pp.1017-1024
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• 2007

Thymus and activation-regulated chemokine (TARC/CCL-17), produced by keratinocytes, is a CC chemokine known to selectively Th2 type T cells via $CCR4^+$ and is implicated in the development of atopic dermatitis (AD). TARC/CCL17 expression was induced by cytokines such as tumor necrosis factor-${\alpha}$ (TNF-${\alpha}$) and interferon-${\gamma}$ (IFN-${\gamma}$). We recently found that the wogonin, a flavone isolated from Scutellaria baicalensis, suppressed TARC expression via heme oxygenase 1 (HO1) in human keratinocytes induced with mite antigen. However, little is known about the inhibitory mechanism of wogonin on TARC/CCL-17 expression stimulated with cytokines. To investigate the inhibitory mechanism, I determined the inhibitory effects of wogonin on the activation of nuclear factor-${\kappa}B$ (NF-${\kappa}B$) and $I{\kappa}B{\alpha}$ phosphorylation, and also examined the activation of p38 MAP kainase in HaCaT keratinocytes stimulated with TNF-${\alpha}$ and IFN-${\gamma}$. Wogonin inhibited NF-${\kappa}B$-DNA complex, NF-${\kappa}B$ binding activity, and the phosphorylation of $I{\kappa}B{\alpha}$ in a dose dependent manner. Wogonin also inhibited the translocation of NF-${\kappa}B$ from cytosol to nucleus. Moreover, the phosphorylation of of p38 MAP kinase in the TNF-${\alpha}$ and IFN-${\gamma}$-stimulated HaCaT keratinocytes were suppressed by wogonin in a dose dependent manner. These results suggest that wogonin may inhibit cytokine-induced NF-${\kappa}B$ activation by $I{\kappa}B{\alpha}$ degradation via suppression of p38 MAP kinase signaling pathway in keratinocytes and modulation of wogonin signaling pathway may be beneficial for the treatment of AD.

• 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.

• Journal of Ginseng Research
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• v.37 no.3
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• pp.315-323
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• 2013

Ginseng is known to have antistress effects. Previously, red ginseng (RG) was shown to repress stress-induced peptidyl arginine deiminase type IV (PADI4) via estrogen receptor ${\beta}$ ($ER{\beta}$) in the brain, thus inhibiting brain cell apoptosis. Moreover, tumor necrosis factor (TNF)-${\alpha}$ plays a critical role in immobilization (IMO) stress. However, the signaling pathway of RG-mediated repressesion of inflammation is not completely understood. In this study, we determined how RG modulated gene expression in stressed brain cells. Since secretion of TNF-${\alpha}$ is modulated via TNF-${\alpha}$ converting enzyme (TACE) and nuclear factor (NF)-${\kappa}B$, we examined the inflammatory pathway in stressed brain cells. Immunohistochemistry revealed that TACE was induced by IMO stress, but RG repressed TACE induction. Moreover, PADI4 siRNA repressed TACE expression compared to the mock transfected control suggesting that PADI4 was required for TACE expression. A reporter assay also revealed that $H_2O_2$ oxidative stress induced NF-${\kappa}B$ in neuroblastoma SK-N-SH cells, however, RG pretreatment repressed NF-${\kappa}B$ induction. These findings were supported by significant induction of nitric oxide and reactive oxygen species (ROS) by oxidative stress, which could be repressed by RG administration. Taken together, RG appeared to repress stress-induced PADI4 via TACE and NF-${\kappa}B$ in brain cells thus preventing production of ROS and subsequently protecting brain cells from apoptosis.

• Journal of Digital Convergence
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• v.11 no.12
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• pp.639-647
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• 2013

This paper is a methodological research aimed at developing a mental disorder recovery scale (MDRS) and testing its validity and reliability. After three sessions of factor analysis, a total of three factors using an Eigen value of 1.0 or more were drawn. The explanatory power was found to be 58.1%. All the items met the criteria for communality and factor loading with no item removed, and, ultimately, 25 items were selected. Criterion-related validity test showed that Pearson's correlation coefficient was significant at .71 (p<.01) with significant correlation with each factor (p<.01). The reliability test showed that Cronbach's ${\alpha}$ coefficient was .95 and that Cronbach's ${\alpha}$ coefficient for each factor ranged from .87 to .93. MDRS, which was developed in this study and possessing 3 factors and 25 items, had both its validity and reliability confirmed; therefore, the developed scale would be useful to evaluate the recovery of individuals with mental disorder.

• CELLMED
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• v.2 no.3
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• pp.27.1-27.6
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• 2012

Red ginseng, which has a variety of biological and pharmacological activities including antioxidant, anti-inflammatory, antimutagenic and anticarcinogenic effects, has been used for thousands of years as a general tonic in traditional oriental medicine. Here, we tested the immune regulatory activities of hydrolyzed red ginseng by malted barley (HRG) on the expressions of receptor interacting proteins (Rip) 2 and $I{\kappa}B$ kinase-beta (IKK-${\beta}$) in mouse peritoneal macrophages. We show that HRG increased the activations of Rip 2 and IKK-${\beta}$ for the first time. When HRG was used in combination with recombinant interferon-${\gamma}$ (rIFN-${\gamma}$), there was a marked cooperative induction of nitric oxide (NO) production. The increased expression of inducible NO synthase from rIFN-${\gamma}$ plus HRG-stimulated cells was almost completely inhibited by pre-treatment with pyrrolidine dithiocarbamate (PDTC), an inhibitor of nuclear factor-${\kappa}B$ (NF-${\kappa}B$). In addition, the treatment of peritoneal macrophages with rIFN-${\gamma}$ plus HRG caused significant increases in tumor necrosis factor (TNF)-${\alpha}$ mRNA expression and production. Because NO and TNF-${\alpha}$ play an important role in the immune function and host defense, HRG treatment can modulate several aspects of the host defense mechanisms as a result of the stimulations of the inducible nitric oxide synthase and NF-${\kappa}B$. In conclusion, our findings demonstrate that HRG increases the productions of NO and TNF-${\alpha}$ from rIFN-${\gamma}$-primed macrophages and suggest that Rip2/IKK-${\beta}$ plays a critical role in mediating these immune regulatory effects of HRG.

• Applied Biological Chemistry
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• v.38 no.1
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• pp.63-66
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• 1995

Soybean nuclear extracts were prepared to detect SEF3(soybean embryo factor 3), which is presumed to be a trans-acting factor for the expression of the soybean ${\beta}-conglycinin\;{\alpha}'$ subunit gene. To increase the specific activity of DNA probe during labeling with $[{\alpha}-^{32}P]$dATP, dATP was added to a final concentration of 1.1 mM during the chase reaction. It results in approximately four-fold increase of specific activity of the DNA probe. Effects of several modifications in preparation of soybean nuclear extracts were examined. It was found that glycerol is effective to stabilize SEF3 during the preparation of nuclear extracts and polyethylenimine could be used to increase the specific activity of SEF3 in nuclear extracts.

• Biomolecules & Therapeutics
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• v.25 no.4
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• pp.383-389
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• 2017

Dexmedetomidine is an ${\alpha}2$-adrenergic receptor agonist that exhibits a protective effect on ischemia-reperfusion injury of the heart, kidney, and other organs. In the present study, we examined the neuroprotective action and potential mechanisms of dexmedetomidine against ischemia-reperfusion induced cerebral injury. Transient focal cerebral ischemia-reperfusion injury was induced in Sprague-Dawley rats by middle cerebral artery occlusion. After the ischemic insult, animals then received intravenous dexmedetomidine of $1{\mu}g/kg$ load dose, followed by $0.05{\mu}g/kg/min$ infusion for 2 h. After 24 h of reperfusion, neurological function, brain edema, and the morphology of the hippocampal CA1 region were evaluated. The levels and mRNA expressions of interleukin-$1{\beta}$, interleukin-6 and tumor nevrosis factor-${\alpha}$ as well as the protein expression of inducible nitric oxide synthase, cyclooxygenase-2, nuclear factor-${\kappa}Bp65$, inhibitor of ${\kappa}B{\alpha}$ and phosphorylated of ${\kappa}B{\alpha}$ in hippocampus were assessed. We found that dexmedetomidine reduced focal cerebral ischemia-reperfusion injury in rats by inhibiting the expression and release of inflammatory cytokines and mediators. Inhibition of the nuclear factor-${\kappa}B$ pathway may be a mechanism underlying the neuroprotective action of dexmedetomidine against focal cerebral I/R injury.

• Asian Pacific Journal of Cancer Prevention
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• v.17 no.4
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• pp.1649-1654
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• 2016

Tea derived from the leaves and buds of Camellia sinensis (Theaceae) is consumed worldwide. Green tea contains various components with specific health-promoting effects, and is believed to exert protective effects against diseases including cancer, diabetes and hepatitis, as well as obesity. Of the various tea components, the polyphenol catechins have been the subject of extensive investigation and among the catechins, (-)-epigallocatechin gallate has the strongest bioactivity in most cases. Our research group has postulated that hepatocyte nuclear factor-$4{\alpha}$, sterol regulatory element-binding proteins, and tumor necrosis factor-${\alpha}$ are targets of green tea constituents including (-)-epigallocatechin gallate for their anti-diabetes, anti-obesity, and anti-hepatitis effects, respectively. Published papers were reviewed to determine whether the observed changes in these factors can be correlated with anti-cancer effects of green tea. Two major action mechanisms of (-)-epigallocatechin gallate have been proposed; one associated with its anti-oxidative properties and the other with its pro-oxidative activity. When reactive oxygen species are assumed to be involved, our findings that (-)-epigallocatechin gallate downregulated hepatocyte nuclear factor-$4{\alpha}$, sterol regulatory element-binding proteins, and tumor necrosis factor-${\alpha}$ may explain the anti-cancer effect of green tea as well. However, further studies are required to elucidate which determinant directs (-)-epigallocatechin gallate action as an anti-oxidant or a pro-oxidant for favorable activity.

• Journal of Ginseng Research
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• v.37 no.2
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• pp.187-193
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• 2013

The effect of Korean red ginseng (KRG) on diabetic renal damage was investigated using streptozotocin (STZ)-induced diabetic rats. The diabetic rats showed loss of body weight gain, and increases in kidney weight and urine volume, whereas the oral administration of KRG at a dose of 100 or 250 mg/kg of body weight per day for 28 d prevented these diabetes-induced physiological abnormalities. Among the kidney function parameters, elevated plasma levels of urea nitrogen and creatinine in diabetic control rats tended to be lowered in KRG-treated rats. In addition, administration of KRG at a dose of 100 mg/kg body weight in the diabetic rats showed significant decreases in serum glucose and tumor necrosis factor-${\alpha}$ (TNF-${\alpha}$), implying that KRG might prevent the pathogenesis of diabetic complications caused by impaired glucose metabolism and oxidative stress. KRG also significantly reduced advanced glycation end product (AGE) formation and secretion from kidney of diabetic rats. Furthermore, KRG decreased the levels of N-(carboxymethyl) lysine and expression of AGE receptor. KRG also reduced the overexpression of cyclooxygenase-2 and inducible nitric oxide synthase in the kidney via deactivation of nuclear factor-kappa B. We also found that KRG prevented STZ-induced destruction of glomerular structure and significantly suppressed high glucose-induced fibronectin production. Taken together, KRG ameliorates abnormalities associated with diabetic nephropathy through suppression of inflammatory pathways activated by TNF-${\alpha}$ and AGEs. These findings indicate that KRG has a beneficial effect on pathological conditions associated with diabetic nephropathy.