• KSBB Journal
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• v.28 no.1
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• pp.7-12
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• 2013

Thromboxane $A_2$ ($TXA_2$) is one of major proinflammatory mediators, plays an important role in the development of vascular inflammatory diseases. $TXA_2$ acting through the thromboxane receptor regulates multiple pathways and genes in a variety of cells. In this study, we report that the activation of thromboxane receptor with U46619 increases the interleukin-8 (IL-8) mRNA in vascular endothelial cells. We also demonstrated that U46619 produces the activations of extracellular signal-regulated kinase 1/2 (ERK1/2) and p38 mitogen-activated protein kinase (MAPK), which is required for endothelial IL-8 production. And U46619 enhanced mRNA stability of IL-8 transcripts in endothelial cells. Moreover, inhibition of ERK1/2 or p38MAPK reduced monocyte adhesion to aortic endothelium stimulated by U46619. Therefore, these results suggest that activation of thromboxane receptor promotes the expression of IL-8 via ERK1/2 and p38MAPK activation in endothelial cells.

• The Journal of Korean Medicine Ophthalmology and Otolaryngology and Dermatology
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• v.20 no.1 s.32
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• pp.99-114
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• 2007

Objectives : Atopic dermatitis has a close relationship with damage of skin barrier function. To investigate the effects of Bangpungtongsungsan(BT) extract to the skin damage on mice model after atopic dermatitis elicitation, this study was done through forcing injury to mice's skin. Methods : The BALB/c mice were distributed into three groups: control(CON) group, atopic dermatitis(AD)-elicited group, Bangpungtongsungsan(BT)-treated group. AD-elicited and BT-treated group were caused AD according to the method of Christophers E., Mrowietz and Minehiro. The BT extract was administered for 48 hours to BT-treated group. We observed changes of external dermal formation, eosinophils in vasculature, lipid formation in stratum corneum, distribution of ceramide, distribution of capillary, $I{\kappa}B$ kinase(IKK) and induce nitric oxide synthase(iNOS) mRNA expression. We used the statistical methods of student t-test(p<0.05). Results : After dispensing BT extract into the AD-elicited group, the number of eosinophil as an atopic index in mice noticeably decreased and dermal injury decreased. Also the decrease of hyperplasia, degranulated mast cells, angiogenesis and substance P were shown. The lipid lamellae, lipid protect formation, were repaired and the distribution of ceramide which inhibit protein kinase C(PKC) activation increased, and the PKC caused inhibition of nuclear $factor(NF)-{\kappa}B$ activation. As a result of inhibition of $NF-{\kappa}B$ activation, iNOS production were inhibited and apoptotic cell were increased. Moreover the decrease of IKK and iNOS mRNA expression in BT-treated RAW 264.7 cell were noted. Conclusion : BT mitigated skin damage on mice model after atopic dermatitis elicitation through recovering skin barrier function and inhibiting nuclear $factor(NF)-{\kappa}B$ activation.

• Journal of the Korean Society of Food Science and Nutrition
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• v.44 no.5
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• pp.649-656
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• 2015

The protective effect of zinc against cortisol-induced cell injury was examined in rainbow trout gill epithelial cells. Cells exposed to cortisol for 24 h showed increased leakage of lactate dehydrogenase (LDH) as well as decreased cell viability in a dose-dependent manner. Treatment with zinc ($100{\mu}M$ $ZnSO_4$) reduced the severity of both LDH release and cell death as well as protected cells against cortisol-induced caspase-3 activation, indicating reduction of apoptosis. Cortisol-induced cell death, leakage of LDH, and caspase-3 activation were blocked by the glucocorticoid receptor antagonist Mifepristone (RU-486), suggesting that cell injury was cortisol-dependent. In addition, we studied the effect of zinc on the expression of antioxidant genes such as metallothionein A (MTA), metallothionein B (MTB), glutathione-S-transferase (GST), and glucose-6-phosphate dehydrogenase (G6PD) during cortisol-induced cell injury. MTA, MTB, GST, and G6PD mRNA levels increased after treatment with zinc or cortisol, separately or in combination. Higher mRNA levels of MTA, MTB, GST, and G6PD were detected when cells were treated with $100{\mu}M$ $ZnSO_4$ and $1{\mu}M$ cortisol in combination at the same time compared to treatment with zinc or cortisol separately. Cells treated with zinc showed increased intracellular free zinc concentrations, and this response was significantly enhanced in cells treated with cortisol and zinc. In conclusion, zinc treatment inhibited cortisol-induced cytotoxicity and apoptosis through indirect antioxidant action.

• BMB Reports
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• v.49 no.2
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• pp.93-98
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• 2016

Germline stem cells (GSCs) are the best understood adult stem cell types in the nematode Caenorhabditis elegans, and have provided an important model system for studying stem cells and their cell fate in vivo, in mammals. In this review, we propose a mechanism that controls GSCs and their cell fate through selective activation, repression and mobilization of the specific mRNAs. This mechanism is acutely controlled by known signal transduction pathways (e.g., Notch signaling and Ras-ERK MAPK signaling pathways) and P granule (analogous to mammalian germ granule)-associated mRNA regulators (FBF-1, FBF-2, GLD-1, GLD-2, GLD-3, RNP-8 and IFE-1). Importantly, all regulators are highly conserved in many multi-cellular animals. Therefore, GSCs from a simple animal may provide broad insight into vertebrate stem cells (e.g., hematopoietic stem cells) and their cell fate specification.

• Proceedings of the Korean Biophysical Society Conference
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• 2001.06a
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• pp.65-65
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• 2001

We have recently demonstrated that high glucose (50 mM D-glucose) upregulates fibronectin mRNA expression and protein synthesis by human peritoneal mesothelial cells (HPMC) through activation of protein kinase C (PKC) and suggested that this may lead to progressive peritoneal fibrosis during a long-term peritoneal dialysis (PD) using glucose as an osmotic agent.(omitted)

• International Journal of Oral Biology
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• v.31 no.1
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• pp.21-26
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• 2006

Periodontopathogens including Porphyromonas gingivalis interact with host periodontal cells and the excessive subsequent host responses contribute a major part to the development of periodontal diseases. Cyclooxygenase(COX)-2-synthesized $PGE_2$ has detrimental activities in terms of periodontal pathogenesis. The present study investigated induction of COX-2 expression by P. gingivalis in human monocytic THP-1 cells. Live P. gingivalis increased expression of COX-2, but not that of COX-1, which was demonstrated at both mRNA and protein levels. Elevated levels of $PGE_2$ were released from P. gingivalis-infected THP-1 cells. Pharma-cological inhibition of p38 mitogen-activated protein kinase(MAPK) and extracellular signal-regulated kinase(ERK) substantially attenuated P. gingivalis-induced COX-2 mRNA expression. Indeed, activation of p38 MAPK and ERK was observed in P. gingivalis-infected THP-1 cells. Also, P. gingivalis induced activation of nuclear $factor-{\kappa}B\;(NF-{\kappa}B)$ which is an important transcription factor for COX-2. These results suggest that COX-2 expression is up regulated in P. gingivalis-infected monocytic cells, at least in part, via p38 MAPK, ERK, and $NF-{\kappa}B$.

• Biomedical Science Letters
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• v.16 no.4
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• pp.239-246
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• 2010

It is suggested that ovariectomy induces body weight gain primarily in the form of adipose tissue in rodents. Since liver peroxisome proliferator-activated receptor ${\alpha}$ (PPAR${\alpha}$) and uncoupling 2 (UCP2) are involved in the regulation of energy expenditure, it was investigated whether swim training regulates ovariectomy-induced adiposity and steatosis through liver PPAR${\alpha}$ and UCP2 activation in female ovariectomized mice, an animal model of postmenopausal women. Swim-trained mice had significantly decreased adipose tissue weights compared with sedentary control mice. Histological analysis showed that hepatic lipid accumulation was inhibited by swim training. Concomitantly, swim training significantly increased mRNA levels of PPAR${\alpha}$ and its target genes responsible for peroxisomal fatty acid ${\beta}$-oxidation, such as acyl-CoA oxidase, enoyl-CoA hydratase/3-hydroxyacyl-CoA dehydrogenase and thiolase in the liver. Moreover, swim training induced the mRNA expression of UCP2. These results suggest that swim training can effectively prevent adiposity and steatosis caused by ovariectomy, in part through activation of liver PPAR${\alpha}$ and UCP2 in female obese mice.

• Biomedical Science Letters
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• v.17 no.1
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• pp.13-20
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• 2011

The peroxisome proliferator-activated receptor ${\alpha}$ ($PPAR{\alpha}$) is a nuclear transcription factor that plays a central role in lipid and lipoprotein metabolism. To investigate whether swim training improves obesity and lipid metabolism through $PPAR{\alpha}$ activation in female sham-operated (Sham) and ovariectomized (OVX) mice, we measured body weight, visceral adipose tissue mass, serum free fatty acid at 6 weeks as well as the expression of hepatic $PPAR{\alpha}$ target genes involved in fatty acid oxidation. Swim-trained mice had decreased body weight, visceral adipose tissue mass and serum free fatty acid levels compared to high fat diet fed control mice in both female Sham and OVX mice. These reductions were more prominent in OVX than in Sham mice. Swim training significantly increased hepatic mRNA levels of $PPAR{\alpha}$ target genes responsible for mitochondrial fatty acid ${\beta}$-oxidation, such as carnitine palmitoyltransgerase-1 (CPT-1), very long chain acyl-CoA dehydrogenase (VLCAD), and medium chain acyl-CoA dehydrogenase (MCAD) in OVX mice. However, swim trained female Sham mice did not increase hepatic mRNA levels of $PPAR{\alpha}$ target genes responsible for mitochondrial fatty acid ${\beta}$-oxidation compared to Sham control mice. These results indicate that swim training differentially regulates body weight and adipose tissue mass between OVX and Sham mice, at least in part due to differences in liver $PPAR{\alpha}$ activation.

• International Journal of Oral Biology
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• v.38 no.2
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• pp.67-72
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• 2013

This study examined the anti-osteoclastogenic effects of baicalin on receptor activator of NF-${\kappa}$B ligand (RANKL)-induced RAW264.7 cells. Baicalin is a flavonoid that is produced by Scutellaria baicalensis and is known to have multiple biological properties, including antibacterial, anti-inflammatory and analgesic effects. The effects of baicalin on osteoclasts were examined by measuring 1) cell viability; 2) the formation of tartrate-resistant acid phosphatase (TRAP) (+) multinucleated cells; 3) RANK/RANKL signaling pathways and 4) mRNA levels of osteoclast-associated genes. Baicalin inhibited the formation of RANKL-stimulated TRAP (+) multinucleated cells and also suppressed the RANKL-stimulated activation of p-38, ERK, cSrc and AKT signaling. Baicalin also inhibited the RANKL-stimulated degradation of $I{\kappa}B$ in RAW264.7 cells. In addition, the RANKL-stimulated induction of NFATc1 transcription factors was found to be abrogated by this flavonoid. Baicalin was further found to decrease the mRNA expression of osteoclast-associated genes, including carbonic anhydrase II, TRAP and cathepsin K in the RAW264.7 cells. Our data thus demonstrate that baicalin inhibits osteoclastogenesis by inhibiting the RANKL-induced activation of signaling molecules and transcription factors in osteoclast precursors.

• The Journal of Korean Obstetrics and Gynecology
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• v.30 no.4
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• pp.1-17
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• 2017

Objectives: This study was conducted to evaluate the effects of Hyeolbuchugeo-tang (HBC) on Osteoporosis. Methods: We induced RAW 264.7 cells to differentiate to Osteoclasts by RANKL and treated RANKL-induced RAW 264.7 cells with HBC (0, 150, 350, $700{\mu}g/ml$). To measure osteoclast differentiation and activation, we counted TRAP (+) MNCs and measured mRNA expressions of its related genes (TRAP, MMP-9, cathepsin K, NFATc1, c-Fos, MITF, iNOS, COX-2, TNF-${\alpha}$) by RT-PCR. To assess bone resorption, the Bone pit formation were examined under a microscope. Results: HBC decreased TRAP (+) MNCs and inhibited mRNA expressions of TRAP, MMP-9, cathepsin K, NFATc1, c-Fos, MITF in osteoclast. And HBC inhibited Bone pit formation. Conclusions: HBC inhibited osteoclast differentiation and activation and bone resorption. Taken together, these results indicate that HBC might have potentials for prevention and treatment of Osteoporosis.