• 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.

• Journal of Physiology & Pathology in Korean Medicine
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• v.22 no.3
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• pp.660-665
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• 2008

In the present study, we investigated the anti-allergic effect of the water extract of Bopyeoyangyeong-jun(BYJ). To investigate the biological effect of BYJ, We examined cytotoxicity and inflammatory cytokine secretion with RBL-2H3. We examined Cell Viability, ${\beta}$-hexosaminidase, tumor necrosis factor-alpha(TNF-${\alpha}$), interleukin(IL)-4 secretion from RBL-2H3 cell after pre- treatment with Bopyeoyangyeong-jun of 1 mg/ml, 2 mg/ml. RBL-2H3 cell was stimulated with phorbol 12-myristate 13-acetate(PMA) and calcium ionophore A23187. BYJ by itself had no effect on viability of RBL-2H3 cell. We observed that Bopyeoyangyeong-jun reduced ${\beta}$-hexosaminidase, TNF-${\alpha}$, IL-4 secretion in RBL-2H3 cell. Taken together, these results indicate that Bopyeoyangyeong-jun has anti-histamic effect and controls TNF-${\alpha}$, IL-4 secretion on allergic reaction.

• YAKHAK HOEJI
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• v.54 no.6
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• pp.500-506
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• 2010

TNF-${\alpha}$ and VCAM-1 play a pivotal role in the pathogenesis of rheumatoid arthritis, and the development of drugs targeting these molecules has extended the therapeutical approaches to rheumatoid arthritis patients. Bispecific antibodies combine the antigen-binding sites of two antibodies within a single molecule and thus they are able to bind to two different epitopes simultaneously. A specific bispecific antibody format termed "Di-diabody" was made for the efficient approach to anti-inflammation. In this study, the DNA vector construct of Di-diabody was built up against two antigens, VCAM-1 and TNF-${\alpha}$. For evaluating this Di-diabody as a bispecific antibody on the efficacy of anti-inflammation, the proteins were analyzed according to each antigen binding affinity and cell based assay related separate molecules. The 7H/Humira Di-diabody produced in this study interacted with its ligands, VCAM-1 and TNF-${\alpha}$, respectively. Also, this antibody exhibited the similar functional activities as compared to 7H-IgG in respect to inhibition of hVCAM-1-induced cell adhesion and Humira-IgG in respect to inhibition of TNF-${\alpha}$ induced cytotoxicity. Further study to elucidate the pharmacological significance of the Di-diabody is warranted using experimental animals.

• 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.

• Archives of Pharmacal Research
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• v.26 no.9
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• pp.731-734
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• 2003

Five known kaurane type diterpenoids, 16$\alpha$H, 17-isovaleryloxy-ent-kauran-19-oic acid (1), 16$\alpha$-hydroxy-17-isovaleryloxy-ent-kauran-19-oic acid (2), paniculoside-IV (3), 16$\alpha$-hydroxy-ent-kauran-19-oic acid (4), and ent-kaur-16-en-19-oic acid (5) were isolated from the root of Acanthopanax koreanum by repeated column chromatography and reversed phase preparative HPLC. The structures of these compounds were established from physicochemical and spectral data. Among the isolated compounds 16$\alpha$H, 17-isovaleryloxy-ent-kauran-19-oic acid (1) showed potent inhibitory activity ($IC_50$ value, 16.2 $\mu$ M) on TNF-$\alpha$ secretion from HMC-1, a trypsin-stimulated human leukemic mast cell line.

• The Journal of Pediatrics of Korean Medicine
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• v.30 no.2
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• pp.31-46
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• 2016

Objectives In this study, the effects of Ja-eum-gang-hwa-tang (JGT) on the increase in airway epithelial mucosubstances of rats and ATP- or PMA- or EGF- or TNF-${\alpha}$-induced MUC5AC mucin production and gene expression from human airway epithelial cells were investigated. Materials and Methods Hypersecretion of airway mucus was produced by exposure of $SO_2$ to rats for 3 weeks. The effect of orally-administered JGT for 2 weeks on increased epithelial mucosubstances from tracheal goblet cells of rats was assessed by using histopathological analysis after staining the epithelial tissue with Hematoxylin-eosin and PAS-alcian blue. Possible cytotoxicity of JGT was assessed by investigating the potential damage on kidneys and liver functions by measuring serum GOT/GPT activities and serum BUN concentration of rats and the body weight gain during experiment. Also, the effect of JGT on ATP- or PMA- or EGF- or TNF-${\alpha}$-induced MUC5AC mucin production and gene expression from human airway epithelial cells (NCI-H292) were investigated. Confluent NCI-H292 cells were pretreated for 30 min in the presence of JGT and treated with ATP ($200{\mu}M$) or PMA ($10ng/ml$) or EGF ($25ng/ml$) or TNF-${\alpha}$ (0.2 nM) for 24 hrs to assess the effect of JGT both on ATP- or PMA- or EGF- or TNF-${\alpha}$-induced MUC5AC mucin production by using enzyme-linked immunosorbent assay (ELISA) and on gene expression by the same inducers using reverse transcription-polymerase chain reaction (RT-PCR). Results (1) JGT decreased the amount of intraepithelial mucosubstances of trachea of rats. (2) JGT did not show any renal and hepatic toxicities, and did not affect body weights either. (3) JGT significantly inhibited ATP-, PMA-, EGF-, and TNF-${\alpha}$-induced MUC5AC mucin productions from NCI-H292 cells. (4) JGT inhibited EGF-, and PMA-induced expression levels of MUC5AC gene in NCI-H292 cells. However, ATP- and TNF-${\alpha}$-induced MUC5AC gene expression levels were not affected in NCI-H292 cells. Conclusions The result from the present study suggests that JGT might control the production and gene expression of airway mucin observed in various respiratory diseases which accompanied by mucus hypersecretion. Also, JGT did not show liver toxicity or impact on kidney functions. The effect of JGT should be further studied by using animal experimental models which can show proper pathophysiology of airway diseases.

• Journal of Pharmacopuncture
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• v.6 no.2
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• pp.45-56
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• 2003

Objective : The purpose of this study was to investigate the effects of Bee Venom on the lipopolysaccharide(LPS), sodium nitroprusside(SNP), hydrogen peroxide$(H_2O_2)$-induced expression inducilble nitric oxide synthetase(iNOS), tumor necrosis factor-${\alpha}$(TNF-${\alpha}$) and nuclear factor kappa B(NF-kB) in RAW 264.7 cells, a murine macrophage cell line. Method : The expressions of expression iNOS and TNF-${\alpha}$ were determined by western blotting with corresponding antibodies. The expressions of expression NF-kB was assayed by EMSA method. Results : 1. The 0.5, 1 and $5{\mu}g/mg$ of bee venom on LPS-induced expression of iNOS, the $5{\mu}g/mg$ of bee venom on SNP-induced expression of iNOS and the $1{\mu}g/mg$ of bee venom on $H_2O_2$-induced expression of iNOS compared with control were inhibited significantly. 2. The 0.5, 1 and $5{\mu}g/mg$ of bee venom inhibited significantly LPS and $H_2O_2$-induced expression of TNF-${\alpha}$ compared with control, respectively. The $0.5{\mu}g/mg$ of bee venom increased significantly SNP-induced expression of TNF-${\alpha}$ compared with control. 3. The $5{\mu}g/mg$ of bee venom on LPS-induced expression of NF-kB, the $0.5{\mu}g/mg$ of bee venom on SNP-induced expression of NF-kB and the 0.5, $5{\mu}g/mg$ of bee venom on $H_2O_2$-induced expression of NF-kB were inhibited significantly compared with control, respectively.

• Journal of Pharmacopuncture
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• v.14 no.2
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• pp.15-24
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• 2011

Background: Type I allergy is involved in allergic asthma, allergic rhinitis, and atopic dermatitis which are accompanied by an acute and chronic allergic inflammatory responses. Rehmannia glutinosa is a traditional medicine in the East Asian region. This study examined whether a Rehmannia Glutinosa pharmacopuncture solution (RGPS) had anti-allergic or anti-inflammatory effects in antigen-stimulated-RBL-2H3 cells. Methods: We determined the effect of RGPS on cell viability using the 3-[4,5-dimethylthiazolyl]-2,5-diphenyltetrazolium bromide (MTT) assay. We also examined the effect of RGPS on the release of ${\beta}$-hexosaminidase and the secretion of IL-4 and TNF-${\alpha}$ using ELISA. In addition, we evaluated the effect of RGPS on the mRNA expression of various cytokines; IL-2, IL-3, IL-4, IL-5, IL-13 and TNF-${\alpha}$ using RT-PCR. Furthermore, we assessed the activation of mitogen-activated protein kinases (MAPKs) and nuclear factor (NF)-${\kappa}$B using Western blotting after RGPS treatment. Results: We found that RGPS ($10^{-4}$ to $10^{-1}$ dilution) did not cause any cytotoxicity. We observed significant inhibition of ${\beta}$-hexosaminidase release and suppression of the protein secretion of IL-4 and TNF-${\alpha}$ and mRNA expression of multiple cytokines in antigen-stimulated-RBL-2H3 cells after RGPS treatment. Additionally, RGPS suppressed not only the phosphorylation of MAPKs, but also the transcriptional activation of NF-${\kappa}$B in antigen-stimulated-RBL-2H3 cells. Conclusions: These results suggest that RGPS inhibits degranulation and expression of cytokines including IL-4 and TNF-${\alpha}$ via down-regulation of MAPKs and NF-${\kappa}$B activation in antigen-stimulated-RBL-2H3 cells. In conclusion, RGPS may have beneficial effects in the exerting anti-allergic or anti-inflammatory activities.

• Natural Product Sciences
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• v.18 no.4
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• pp.254-260
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• 2012

Adipose inflammation is linked to the development of insulin resistance and type 2 diabetes. Hesperidin (HES) is a flavonoid with antioxidant, anti-inflammatory and anti-diabetic properties. However, whether HES improves inflammation-mediated insulin resistance in adipose tissues remains unclear. The purpose of this study was to investigate whether HES attenuates inflammation-mediated insulin resistance in adipose tissue. Herein, RAW 264.7 cells and differentiated 3T3-L1 adipocytes were pretreated with various concentrations of HES in complete media for 1 h and then cultured in the presence or absence of LPS or TNF-${\alpha}$. Our results demonstrated that HES remarkably inhibited LPS-induced production of IL-6, TNF-${\alpha}$, and NO by RAW 264.7 cells in a dose-dependent manner. Also, HES inhibited TNF-${\alpha}$-induced production of IL-6 and $PGE_2$ in differentiated 3T3-L1 cells, while upregulated TNF-${\alpha}$-suppressed expression of adiponectin and PPAR-${\gamma}$ mRNA. These findings suggest that HES may ameliorate inflammation-mediated insulin resistance in adipose tissue.

• Natural Product Sciences
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• v.19 no.4
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• pp.316-323
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• 2013

Adipose tissue-derived chronic inflammation contributes to development of insulin resistance in obesity, leading to type 2 diabetes and cardiovascular disease. Baicalin, a flavonoid, has antioxidant, anti-inflammatory, antihyperglycemic, anti-adipogenic, and antiobesity effects. However, whether baicalin attenuates adipose tissue-derived development of insulin resistance remains still unclear. This study was to investigate effect of baicalin on the inflammatory changes involved in the development of insulin resistance in adipose tissue. RAW 264.7 cells and differentiated 3T3-L1 adipocytes were pretreated with various concentrations of baicalin in complete media for 1 h and then cultured in the presence or absence of LPS or TNF-${\alpha}$. Our results demonstrated that baicalin remarkably inhibited LPS-induced production of TNF-${\alpha}$, IL-6, and NO by RAW 264.7 cells in a dose-dependent manner. Baicalin also inhibited TNF-${\alpha}$-induced production of IL-6 and $PGE_2$ in differentiated 3T3-L1 cells in a dose-dependent manner, while upregulated TNF-${\alpha}$-suppressed expression of adiponectin and PPAR-${\gamma}$ mRNA and IRS-1 protein. These findings suggest that baicalin may prevent the adipose tissue-derived development of insulin resistance in obesity.