• Animal cells and systems
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• v.10 no.2
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• pp.73-77
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• 2006

Caspase-11 has been known as a dual regulator of apoptosis and inflammatory response. An unusual feature of caspase-11 is that its expression is induced by apoptotic or proinflammatory stimuli. Utilizing these unusual features of caspase-11, we have developed a simple and sensitive assay method to screen pro- or anti-apoptotic/inflammatory molecules. To develop this assay method, we generated a reporter construct where GFP expression is regulated by caspase-11 promoter. When several types of cultured cells were transfected with this reporter construct and subsequently treated with various apoptotic or proinflammatory molecules, expression of GFP by the activation of caspase-11 promoter was easily detected by fluorescence microscopy or spectrofluorometry. In addition, a reduction of the GFP fluorescence was detected when an agent reported to suppress caspase-11 induction was applied. These results suggest that our reporter system can be used to screen pro- or anti-apoptotic/inflammatory molecules.

• Proceedings of the Korean Society of Toxicology Conference
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• 2003.10b
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• pp.139-140
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• 2003

Inflammatory as well as oxidative tissue damage has been implicated in pathophysiology of Alzheimer's disease (AD), and non-steroidal anti-inflammatory drugs have been reported to have beneficial effects in the treatment or prevention of AD. In the present study, we investigated the effect of celecoxib, a selective cyclooxygenase-2 (COX-2) inhibitor, on inflammatory cell death induced by beta-amyloid, a neurotoxic peptide associated with senile plaques formed in the brains of patients with AD.(omitted)

• Proceedings of the KTCVS Conference
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• 1998.10a
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• pp.17-17
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• 1998

• Proceedings of the PSK Conference
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• 2000.10a
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• pp.244.3-245
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• 2000

• Proceedings of the PSK Conference
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• 2001.04a
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• pp.152.2-152.2
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• 2001

• Journal of the Korea Convergence Society
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• v.8 no.1
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• pp.239-243
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• 2017

This study aims to demonstrate the inhibitory effect of proinflammatory cytokines by using Frankinsense. The present data was designed to determine the production of the frankincence on pro-inflammatory factors such as $TNF-{\alpha}$ and $IL-1{\beta}$ in lipopolysaccharide(LPS) stimulated RAW264.7 macrophages cell. The cell toxicity was identified by CellTiter 96 AQueous One solution cell proliferation assay. To evaluate of anti-inflammatory effect of frankincence, pro-inflammatory cytokines were measured by ELISA kit. As a result, the frankincence reduced NO and $TNF-{\alpha}$ production without cytotoxicity. As a result, Francincense was not cytotoxic at 10 ug / ml-1000 ug / ml and significantly inhibited the proinflammatory cytokines $TNF-{\alpha}$ and $IL-1{\beta}$. The secretion inhibition effect of proinflammatory cytokine is believed to be applicable to various physiological activity data and functional materials to demonstrate the anti - inflammatory properties of frankincense.

• Korean Journal of Veterinary Research
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• v.49 no.4
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• pp.345-349
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• 2009

Polychlorinated biphenyls (PCBs) are synthetic organic compounds with two benzene rings and well known environmental pollutants. This study examined the effect of persistent exposure to 2,$3^{\prime}$,4,$4^{\prime}$,5-pentachlorobiphenyl (PCB118) on the proinflammatory and proapoptotic factors in male rats. Male Sprague Dawley rats were administered weekly intraperitoneal injections of either PCB118 (20 mg/kg) dissolved in corn oil or corn oil alone. One week after 2 and 5 administrations, the rats were sacrificed by a pentobarbital injection. The effect of PCB118 on the expression of cyclooxygenase 2 (COX-2), cytosolic phospholipase A2 (cPLA2), peroxisome proliferator-activated receptor gamma, Bcl and Bcl-2-associated X protein (BAX) was investigated. The level of COX-2 and cPLA2 expression was higher in the PCB118-treated rats than the control. These results suggest that PCB118 has a proinflammatory effect in rats.

• IMMUNE NETWORK
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• v.10 no.4
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• pp.135-143
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• 2010

Background: Cordyceps militarys water extract (CME) has been reported to exert antitumor and immunomodulatory activities in vivo and in vitro. However, the therapeutic mechanism has not yet been elucidated. In this study, we examined the effects of CME on the antigen presenting function of antigen presenting cells (APCs). Methods: Dendritic cells (DCs) were cultured in the presence of CME, and then allowed to phagocytose microspheres containing ovalbumin (OVA). After washing and fixing the efficacy of OVA, peptide presentation by DCs were evaluated using CD8 and CD4 T cells. Also, we confirmed the protein levels of proinflammatory cytokines through western blot analysis. Results: CME enhanced both MHC class I and class II-restricted presentation of OVA in DCs. In addition, the expression of both MHC class I and II molecules was enhanced, but there was no changes in the phagocytic activity of exogenous OVA. Furthermore, CME induced the protein levels of iNOS, COX-2, proinflammatory cytokines, and nuclear p65 in a concentration-dependent manner, as determined by western blot. Conclusion: These results provide an understanding of the mechanism of the immuno-enhancing activity of CME on the induction of MHC-restricted antigen presentation in relation to their actions on APCs.

• The Journal of the Korean Society for Microbiology
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• v.35 no.1
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• pp.41-48
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• 2000

Bacteroides fragilis and Escherichia coli, normal colonic inhabitants, are the most frequently isolated bacteria in infected tissues, particularly in intraabdominal abscesses. This study was designed to determine whether enteric bacteria may alter the B. fragilis-induced expression of pro inflammatory cytokines in mouse peritoneal tissue (MPT). After C57BL/6 mice were inoculated with abscess-forming mixture containing B. fragilis in the presence or absence of E. coli, RNA was extracted from MPT. Expression of interleukin (IL)-$1{\alpha}$ and tumor necrosis factor $(TNF){\alpha}$ mRNA was assessed using RT-PCR and standard RNA. Each cytokine protein was also measured by ELISA. The co-inoculation of E. coli into mouse peritoneal cavity advanced the onset of abscess development by B. fragilis infection. When mouse was co-infected with E. coli and B. fragilis intraperitoneally, there was a synergistic increase in the expression of IL-$1{\alpha}$ and $TNF{\alpha}$ mRNA in MPT and this was paralleled by increased cytokine protein secretion. Mixed inoculation of heat-killed E. coli and B. fragilis did not cause a synergistic increase in those cytokine mRNA expression. These results suggest that enteric bacteria may significantly affect proinflammatory cytokine signal produced by host peritoneal cavity in response to B. fragilis infection.

• Biomolecules & Therapeutics
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• v.26 no.2
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• pp.210-217
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• 2018

Neuroinflammation is an immune response within the central nervous system against various proinflammatory stimuli. Abnormal activation of this response contributes to neurodegenerative diseases such as Parkinson disease, Alzheimer's disease, and Huntington disease. Therefore, pharmacologic modulation of abnormal neuroinflammation is thought to be a promising approach to amelioration of neurodegenerative diseases. In this study, we evaluated the synthetic flavone derivative 3',4'-dihydroxyflavone, investigating its anti-neuroinflammatory activity in BV2 microglial cells and in a mouse model. In BV2 microglial cells, 3',4'-dihydroxyflavone successfully inhibited production of chemokines such as nitric oxide and prostaglandin $E_2$ and proinflammatory cytokines such as tumor necrosis factor alpha, interleukin 1 beta, and interleukin 6 in BV2 microglia. It also inhibited phosphorylation of mitogen-activated protein kinase (MAPK) and nuclear factor $(NF)-{\kappa}B$ activation. This indicates that the anti-inflammatory activities of 3',4'-dihydroxyflavone might be related to suppression of the proinflammatory MAPK and $NF-{\kappa}B$ signaling pathways. Similar anti-neuroinflammatory activities of the compound were observed in the mouse model. These findings suggest that 3',4'-dihydroxyflavone is a potential drug candidate for the treatment of microglia-related neuroinflammatory diseases.