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Mo, J.-H.,Kang, E.-K.,Quan, S.-H.,Rhee, C.-S.,Lee, C. H.,Kim, D.-Y. Wiley (Blackwell Publishing) 2011 Allergy Vol.66 No.2
<P>To cite this article: Mo J-H, Kang E-K, Quan S-H, Rhee C-S, Lee CH, Kim D-Y. Anti-tumor necrosis factor-alpha treatment reduces allergic responses in an allergic rhinitis mouse model. Allergy 2011; 66: 279-286. ABSTRACT: Background:??Tumor necrosis factor (TNF)-관 is a principal mediator of the acute inflammatory response, including allergic rhinitis. TNF-관 inhibitors are widely used for the treatment of inflammatory conditions such as rheumatoid arthritis and inflammatory bowel diseases; however, the effects of TNF-관 inhibitors on allergic rhinitis are not well established. We aimed to investigate the effects of infliximab, a TNF-관 inhibitor, on allergic rhinitis in a mouse model. Methods:??BALB/c mice were sensitized with ovalbumin (OVA) and alum, and challenged intranasally with OVA. The TNF-관 inhibitor, infliximab was administered intraperitoneally, and multiple parameters of allergic responses were evaluated to determine the effects of infliximab. Results:??Infliximab reduced allergic symptoms and eosinophilic infiltration into the nasal mucosa. It also suppressed total and OVA-specific IgE levels, and inhibited local Th2 cytokine transcription in the nasal mucosa and systemic Th2 cytokine production by splenocytes. Furthermore, the expression of E-selectin, neither intercellular adhesion molecule 1 (ICAM-1) nor vascular cell adhesion molecule 1 (VCAM-1), in the nasal mucosa was suppressed in the infliximab-treated group when compared to the nontreated group. Conclusion:??This study shows that the TNF-관 inhibitor infliximab induces anti-allergic effects by decreasing local and systemic Th2 cytokine (IL-4) production, total and OVA-specific IgE levels, adhesion molecule (E-selectin) expression, and eosinophil infiltration into the nasal mucosa in an allergic rhinitis model. Therefore, infliximab should be considered as a potential agent in treating allergic rhinitis.</P>
Quan, J.H.,Cha, G.H.,Zhou, W.,Chu, J.Q.,Nishikawa, Y.,Lee, Y.H. Academic Press 2013 Experimental parasitology Vol.133 No.4
Toxoplasma gondii-infected cells are resistant to various apoptotic stimuli, however, the role of the pro-apoptotic BH3-only Bad protein in T. gondii-imposed inhibition of host cell apoptosis in connection with the phosphoinositide 3-kinase (PI3K)-PKB/Akt pathway was not well delineated. Here, we investigated the signaling patterns of Bad, Bax and PKB/Akt in T. gondii-infected and uninfected THP-1 cells treated with staurosporine (STS) or PI3K inhibitors. STS treatment, without T. gondii infection, reduced the viability of THP-1 cells in proportion to STS concentration and triggered many cellular death events such as caspase-3 and -9 activation, Bax translocation, cytochrome c release from host cell mitochondria into cytosol, and PARP cleavage in the host cell. However, T. gondii infection eliminated the STS-triggered mitochondrial apoptotic events described above. Additionally, T. gondii infection in vitro and in vivo induced the phosphorylation of PKB/Akt and Bad in a parasite-load-dependent manner which subsequently inhibited Bax translocation. The PI3K inhibitors, LY294002 and Wortmannin, both blocked parasite-induced phosphorylation of PKB/Akt and Bad. Furthermore, THP-1 cells pretreated with these PI3K inhibitors showed reduced phosphorylation of Bad in a dose-dependent manner and subsequently failed to inhibit the Bax translocation, also these cells also failed to overcome the T. gondii-imposed inhibition of host cell apoptosis. These data demonstrate that the PI3K-PKB/Akt pathway may be one of the major route for T. gondii in the prevention of host cell apoptosis and T. gondii phosphorylates the pro-apoptotic Bad protein to prevent apoptosis.
Licochalcone A regulates hepatic lipid metabolism through activation of AMP-activated protein kinase
Quan, H.Y.,Kim, S.J.,Kim, D.Y.,Jo, H.K.,Kim, G.W.,Chung, S.H. Elsevier 2013 Fitoterapia Vol.86 No.-
Licochalcone A (LA) is a major phenolic ingredient of Glycyrrhiza plant. Although multiple pharmacological activities of LA have been reported, effect on hepatic lipid metabolism is unknown yet. The present study showed LA to suppress the hepatic triglyceride accumulation in HepG2 cells and ICR mice fed on a high fat diet (HFD). LA inhibited lipogenesis via suppression of sterol regulatory element-binding protein 1c (SREBP1c) and its target enzymes (stearoyl-CoA desaturase 1, fatty acid synthase and glycerol-3-phosphate acyltransferase) transcription. In addition, LA up-regulated gene expression of proteins such as peroxisome proliferator-activated receptor α (PPARα) and fatty acid transporter (FAT/CD36), which are responsible for lipolysis and fatty acid transport, respectively. These effects were mediated through activation of AMP-activated protein kinase (AMPK), and were abrogated when HepG2 cells were treated with an AMPK inhibitor, compound C. To explore how LA activates AMPK, oxygen consumption rate and ATP levels were measured in HepG2 cells. LA significantly inhibited the mitochondrial respiration and ATP levels, suggesting that LA activated AMPK indirectly. In animal study, LA (5 and 10mg/kg) was orally administered to six-week-old mice once a day for 3weeks. In vitro results were likely to hold true in vivo experiment, as LA markedly lowered the triglyceride levels and activated AMPK signaling pathway in the liver of ICR mice fed on a HFD. In conclusion, the current study suggests that LA suppressed hepatic triglyceride accumulation through modulation of AMPK-SREBP signaling pathway and thus LA may be a potential therapeutic agent for treating fatty liver disease.
Kim, H.J.,Cho, J.H.,Quan, H.,Kim, J.R. North-Holland Pub ; Elsevier Science Ltd 2011 FEBS letters Vol.585 No.22
Aurora B kinase (Aurora-B) functions in chromosome segregation and cleavage of polar spindle microtubules. However, its role in cellular senescence remains elusive. Here, we investigated Aurora-B effects on cellular senescence in human fibroblasts and endothelial cells. Aurora-B levels were reduced during replicative senescence and premature senescence by adriamycin. Aurora-B overexpression in old cells partially reversed senescence phenotypes. In contrast, Aurora-B down-regulation accelerated cellular senescence. p53 knockdown but not p16 knockdown inhibited cellular senescence by Aurora-B reduction. These results suggest that Aurora-B might function in the regulation of cellular senescence of human primary cells via a p53-dependent pathway.