Differences in the relationship between traumatic experiences, self-esteem, negative cognition, and Internet addiction symptoms among North Korean adolescent defectors and South Korean adolescents: A preliminary study

Park, Subin,Lee, Yeeun,Jun, Jin Yong Elsevier/North Holland Biomedical Press 2017 Psychiatry research Vol.257 No.-

<P><B>Abstract</B></P> <P>North Korean adolescent defectors experience adaptation difficulties along with a wide range of psychosocial problems, but no study has yet examined their Internet addiction symptoms. We compared early traumatic experiences, self-esteem, negative cognition, and Internet addiction symptoms, as well as the relationships between these variables, between North Korean adolescent defectors and South Korean adolescents. Fifty-six North Korean adolescent defectors and 112 age- and sex- matched South Korean adolescents participated. The analyses examined the relationship between traumatic experiences and Internet addiction symptoms, with negative automatic thoughts or low self-esteem as mediators of these relations. North Korean adolescent defectors tended to have higher levels of negative automatic thoughts and more severe Internet addiction symptoms, as well as better self-esteem, than did South Korean adolescents. Furthermore, only among North Korean adolescent defectors, traumatic experiences were positively associated with Internet addition symptoms via increasing negative automatic thoughts. North Korean adolescent defectors are more susceptible to Internet addiction, negative cognitions, and early traumatic experiences compared to South Korean adolescents. However, the cross-sectional design of this study precludes consideration of the causality of these relationships. Interventions aiming to correct negative cognitions and increase self-esteem may be helpful for North Korean adolescent defectors with problematic Internet use.</P> <P><B>Highlights</B></P> <P> <UL> <LI> North Korean adolescent defectors had higher trauma and Internet addiction (IA). </LI> <LI> North Korean defectors also had greater self-esteem and negative automatic thoughts. </LI> <LI> Self-esteem and negative thoughts were mediators in the relation of trauma and IA. </LI> <LI> Country of origin (North vs. South Korea) moderated the mediating effects. </LI> </UL> </P>

Stability of uncapped gold nanoparticles produced by laser ablation in deionized water: The effect of post-irradiation

Kim, K.K.,Kwon, H.J.,Shin, S.K.,Song, J.K.,Park, S.M. North Holland ; Elsevier Science Ltd 2013 Chemical physics letters Vol.588 No.-

Gold nanoparticle (AuNP) solution prepared by laser ablation in liquid (LAL) was irradiated by ns laser pulses to investigate the wavelength dependence on the size distribution of AuNPs and long-term stability of post-irradiated AuNP solutions. We have employed 266, 355, 532, and 1064nm lasers for post-irradiation source and found considerable wavelength dependence in the size distribution and stability of laser-generated AuNPs. Post-irradiation at 355nm was most effective to reduce the size distribution and to enhance the stability. The classical Derjaguin-Landau-Verwey-Overbeek theory was employed to explain the anomalous stability at 355nm.

Regulation of ROS-independent ERK signaling rescues replicative cellular senescence in ex vivo expanded human c-kit-positive cardiac progenitor cells

Choi, S.H.,Jung, S.Y.,Yoo, S.Y.,Yoo, S.M.,Kim, D.Y.,Kang, S.,Baek, S.H.,Kwon, S.M. Elsevier/North-Holland Biomedical Press 2013 INTERNATIONAL JOURNAL OF CARDIOLOGY Vol.169 No.1

Backgrounds: Although the rescue of cellular senescence during ex vivo expansion of human-derived cardiac progenitor cells (hCPC) is critical for the application of autologous stem cell therapy in cardiovascular disease, the underlying molecular pathways during replicative senescence in hCPC have not been fully defined. Thus, we examined whether the regulation of mitogen-activated protein kinases activation could facilitate the recovery of human c-kit-positive hCPCs (hCPC<SUP>c-kit+</SUP>) and whether senescence is reactive oxygen species (ROS)-dependent or -independent. Methods and results: To investigate the molecular pathways of replicative cellular senescence, we first evaluated cellular senescence in ex vivo-expanded hCPC<SUP>c-kit+</SUP> by using senescence-associated β-galactosidase (SA-β-gal) activity with enlarged cytoplasm and observed increased expression of cell senescence-related pivotal molecules, including TP53, cleavage Mdm2 (cMdm2), and Mdm2. Unexpectedly, we found that the extracellular signal-regulated kinase (ERK) was markedly activated in aged hCPC<SUP>c-kit+</SUP>, with reduced proliferative activity. SA-β-gal activity and cytoplasm size in senescent hCPC<SUP>c-kit+</SUP> were significantly reduced, with reduced TP53 and cMdm2 expression after treatment with a specific ERK inhibitor (U0126). We examined whether the signaling in ERK inhibitory rescue of hCPC<SUP>c-kit+</SUP> senescence is ROS-dependent. Interestingly, the increased ROS level was not changed after treatment with a specific ERK inhibitor. Similarly, the increased expression levels of endogenous antioxidant enzymes, e.g., peroxiredoxin (Prdx)-1 and 2, in senescent hCPC<SUP>c-kit+</SUP> were not changed after treatment with a specific ERK inhibitor. Conclusions: From the above results, we conclude that the specific inhibition of ERK during cellular senescence might rescue bioactivities of senescent hCPC<SUP>c-kit+</SUP> in a ROS-independent manner.

The natural flavonoid galangin inhibits osteoclastic bone destruction and osteoclastogenesis by suppressing NF-κB in collagen-induced arthritis and bone marrow-derived macrophages

Huh, J.E.,Jung, I.T.,Choi, J.,Baek, Y.H.,Lee, J.D.,Park, D.S.,Choi, D.Y. North-Holland ; Elsevier Science Ltd 2013 european journal of pharmacology Vol.698 No.1

We investigated the effect of galangin, a natural flavonoid, on osteoclastic bone destruction in collagen-induced arthritis and examined the molecular mechanisms by which galangin affects osteoclastogenesis in bone marrow derived macrophages. In mice with collagen-induced arthritis, administration of galangin significantly reduced the arthritis clinical score, edema and severity of disease without toxicity. Interestingly, galangin treatment during a later stage of collagen-induced arthritis, using mice with a higher clinical arthritis score, still significantly slowed the progression of the disease. Extensive cartilage and bone erosive changes as well as synovial inflammation, synovial hyperplasia and pannus formation were dramatically inhibited in arthritic mice treated with galangin. Furthermore, galangin-treated arthritic mice showed a significant reduction in the concentrations of IL-1β, TNF-α and IL-17 . We found that galangin inhibited osteoclastogenic factors and osteoclast formation in bone marrow-derived macrophages and osteoblast co-cultured cells, and increased osteoprotegerin (OPG) levels in osteoblasts. Galangin and NF-κB siRNA suppressed RANKL-induced phosphorylation of the c-jun N-terminal kinase (JNK) and p38 mitogen-activated protein kinase (MAPK), but not AKT and extracellular signal-regulated kinase ½ (ERK½). Also, the JNK inhibitor SP600125 and p38 inhibitor SB203580 reduced RANKL-induced expressions of phospho-c-Jun, c-fos and NFATc1 genes during osteoclast development. In addition, galangin suppressed RANKL-induced phosphorylation of NF-κB, phospho-IκBα, inflammatory cytokines and osteoclast formation in bone marrow-derived macrophages. Our data suggest that galangin prevented osteoclastic bone destruction and osteoclastogenesis in osteoclast precursors as well as in collagen-induced arthritis mice without toxicity via attenuation of RANKL-induced activation of JNK, p38 and NF-κB pathways.

Mechanism underlying anti-hyperalgesic and anti-allodynic properties of anomalin in both acute and chronic inflammatory pain models in mice through inhibition of NF-κB, MAPKs and CREB signaling cascades

Khan, S.,Shehzad, O.,Chun, J.,Kim, Y.S. North-Holland ; Elsevier Science Ltd 2013 european journal of pharmacology Vol.718 No.1

The numerous mediators of pain and inflammation are products of injury-induced gene expression that lead to changes in the nervous system and immune responses. These multiple molecules and mechanisms suggest novel strategies that could be used for analgesic drug development. The present study investigated the possible anti-hyperalgesic effects of anomalin in complete Freund's adjuvant (CFA)-induced acute and chronic inflammatory pain models. Acute pretreatment of mice with anomalin (10 and 50mg/kg, i.p.) produced a significant anti-nociceptive effect against CFA- and carrageenan-induced mechanical hyperalgesia and allodynia. In a chronic pain model, administration of anomalin inhibited CFA-induced hyperalgesia, and it did not cause any apparent toxicity. Another set of experiments observed that anomalin inhibited CFA- and carrageenan-induced paw edema in acute and chronic models. To elucidate the molecular mechanism underlying the anti-nociceptive effect of anomalin, the various pain signaling pathways [NF-κB, cAMP response element-binding protein (CREB), and mitogen activated protein kinase (MAPKs)/AP-1] that are involved were examined. Intraperitoneal (i.p.) pretreatment of anomalin exhibited potent inhibitory effects on direct mediators of hyperalgesia (iNOS and COX-2). The release of CFA-induced plasma nitrite and paw tissue hyperalgesic cytokine (TNF-α) was reduced remarkably. In addition, the adenosine 5'-triphosphate (ATP) in plasma and substance P (SP) in paw tissue were markedly suppressed by anomalin. These results demonstrate that anomalin exhibits an analgesic effect in a consistent manner and that its mechanisms involve the inhibition of the NF-κB, CREB, and MAPKs/AP-1 signaling pathways.

Cardiovascular effects of a novel selective Rho kinase inhibitor, 2-(1H-indazole-5-yl)amino-4-methoxy-6-piperazino triazine (DW1865)

Oh, K.S.,Oh, B.K.,Ho Park, C.,Won Seo, H.,Sook Kang, N.,Hyun Lee, J.,Soo Lee, J.,Ho Lee, B. North-Holland ; Elsevier Science Ltd 2013 european journal of pharmacology Vol.702 No.1

The arising critical implications of Rho kinase signaling in cardiovascular diseases have been attracting attention in the pharmacological potential of Rho kinase inhibitors. We identified a novel inhibitor of Rho kinase (2-(1H-indazole-5-yl)amino-4-methoxy-6-piperazino triazine; DW 1865) and characterized its effects in biochemical, cellular, tissue and animal based assays. DW 1865 potently inhibited the kinase activity of both Rho kinase 1 and Rho kinase 2 in vitro, and behaved as an ATP-competitive inhibitor. Interestingly, DW1865 was 10 times more potent in inhibiting Rho kinase activities than fasudil as a selective Rho kinase inhibitor. The activity of DW1865 was shown to be highly selective for Rho kinase in the panel assay of 13 other kinases. In the isolated vascular tissue study, DW1865 exerted vasorelaxation in phenylephrine- or 5-hydroxytriptamine-induced contraction in a concentration-dependent manner manner. In spontaneously hypertensive rats, administration of DW1865 caused a significant and dose-related reduction in blood pressure. Furthermore, DW1865 blocked angiotensin II-induced stress fiber formation and cellular hypertrophy in rat heart-derived H9c2 cells. Taken together, these results suggest that DW1865 is a highly selective and potent Rho kinase inhibitor that will alleviate the pathophysiological actions of Rho kinase such as stress fiber formation, cellular hypertrophy, and hypertension.

Arctigenin ameliorates inflammation in vitro and in vivo by inhibiting the PI3K/AKT pathway and polarizing M1 macrophages to M2-like macrophages

Hyam, S.R.,Lee, I.A.,Gu, W.,Kim, K.A.,Jeong, J.J.,Jang, S.E.,Han, M.J.,Kim, D.H. North-Holland ; Elsevier Science Ltd 2013 european journal of pharmacology Vol.708 No.1

Seeds of Arctium lappa, containing arctigenin and its glycoside arctiin as main constituents, have been used as a diuretic, anti-inflammatory and detoxifying agent in Chinese traditional medicine. In our preliminary study, arctigenin inhibited IKKβ and NF-κB activation in peptidoglycan (PGN)- or lipopolysaccharide (LPS)-induced peritoneal macrophages. To understand the anti-inflammatory effect of arctigenin, we investigated its anti-inflammatory effect in LPS-stimulated peritoneal macrophages and on LPS-induced systemic inflammation as well as 2,4,6-trinitrobenzene sulfonic acid (TNBS)-induced colitis in mice. Arctigenin inhibited LPS-increased IL-1β, IL-6 and TNF-α expression in LPS-stimulated peritoneal macrophages, but increased LPS-reduced IL-10 and CD204 expression. Arctigenin inhibited LPS-induced PI3K, AKT and IKKβ phosphorylation, but did not suppress LPS-induced IRAK-1 phosphorylation. However, arctigenin did not inhibit NF-κB activation in LPS-stimulated PI3K siRNA-treated peritoneal macrophages. Arctigenin suppressed the binding of p-PI3K antibody and the nucleus translocation of NF-κB p65 in LPS-stimulated peritoneal macrophages. Arctigenin suppressed blood IL-1β and TNF-α level in mice systemically inflamed by intraperitoneal injection of LPS. Arctigenin also inhibited colon shortening, macroscopic scores and myeloperoxidase activity in TNBS-induced colitic mice. Arctigenin inhibited TNBS-induced IL-1β, TNF-α and IL-6 expression, as well as PI3K, AKT and IKKβ phosphorylation and NF-κB activation in mice, but increased IL-10 and CD204 expression. However, it did not affect IRAK-1 phosphorylation. Based on these findings, arctigenin may ameliorate inflammatory diseases, such as colitis, by inhibiting PI3K and polarizing M1 macrophages to M2-like macrophages.

The inhibition of JNK MAPK and NF-κB signaling by tenuifoliside A isolated from Polygala tenuifolia in lipopolysaccharide-induced macrophages is associated with its anti-inflammatory effect

Kim, K.S.,Lee, D.S.,Bae, G.S.,Park, S.J.,Kang, D.G.,Lee, H.S.,Oh, H.,Kim, Y.C. North-Holland ; Elsevier Science Ltd 2013 european journal of pharmacology Vol.721 No.1

The root of Polygala tenuifolia Willd. (Polygalaceae) is well known for its use in the treatment of neurasthenia, amnesia, and inflammation. In this study, we isolated phenyl propanoid type metabolite tenuifoliside A, one of the phenylpropanoids from P. tenuifolia, and investigated its anti-inflammatory effects in lipopolysaccharide (LPS)-stimulated RAW264.7 and murine peritoneal macrophages. The results showed that tenuifoliside A inhibited the production of nitric oxide (NO), inducible nitric oxide synthase (iNOS), prostaglandin E2 (PG E<SUB>2</SUB>), and cyclooxygenase (COX)-2. In addition, tenuifoliside A suppressed the production of pro-inflammatory cytokines, such as tumor necrosis factor (TNF)-α and interleukin (IL)-1β. We also evaluated the effects of tenuifoliside A on the activation of nuclear factor-kappaB (NF-κB). Tenuifoliside A inhibited the translocation of the NF-κB subunit p65 into the nucleus by interrupting the phosphorylation and degradation of inhibitor kappa B (IκB)-α in LPS-stimulated murine peritoneal macrophages. Moreover, we confirmed that the suppression of the inflammatory process by tenuifoliside A was mediated through the mitogen-activated protein kinases (MAPKs) pathway based on the fact that tenuifoliside A significantly decreased p-c-Jun N-terminal kinase (p-JNK) protein expression in LPS-stimulated murine peritoneal macrophages. Taken together, the anti-inflammatory effects of tenuifoliside A were mediated by the inhibition of the NF-κB and MAPK pathways. This study is the first report on the anti-inflammatory effects of tenuifoliside A, and the strong anti-inflammatory effects of tenuifoliside A provide potential compound to be developed as therapeutic for inflammatory diseases.

Ginsenoside Rg₃ regulates GABA_A receptor channel activity: Involvement of interaction with the γ₂ subunit

Lee, B.H.,Kim, H.J.,Chung, L.,Nah, S.Y. North-Holland ; Elsevier Science Ltd 2013 european journal of pharmacology Vol.705 No.1

Ginseng exhibits beneficial effects on GABA<SUB>A</SUB> receptor-related anxiety and sleep disorders. However, little is known regarding the cellular and molecular bases of the ginseng action on GABA<SUB>A</SUB> receptor. The present study was performed to elucidate the molecular mechanism of the ginseng effect on GABA<SUB>A</SUB> receptor. The effect of ginsenoside Rg<SUB>3</SUB> (Rg<SUB>3</SUB>), one of the active ingredients of ginseng, on γ-aminobutyric acid (GABA)<SUB>A</SUB> receptor channel activity was examined in Xenopus oocytes using two-electrode voltage-clamp technique. Rg<SUB>3</SUB> itself evoked an inward current in Xenopus oocytes expressing GABA<SUB>A</SUB> receptor subunits (α<SUB>1</SUB>β<SUB>1</SUB>γ<SUB>2</SUB>) and the Rg<SUB>3</SUB> itself-elicited inward current was only selective to γ<SUB>2</SUB> subunit expression ratio, since Rg<SUB>3</SUB> alone had no effects in oocytes expressing other subunits such as γ<SUB>1</SUB>, γ<SUB>3</SUB>, δ, or ε. Co-treatment of Rg<SUB>3</SUB> with GABA enhanced GABA receptor (α<SUB>1</SUB>β<SUB>1</SUB>γ<SUB>2</SUB>)-mediated inward currents (I<SUB>GABA</SUB>) but Rg<SUB>3</SUB>-mediated I<SUB>GABA</SUB> enhancement was independent on γ<SUB>2</SUB>. Rg<SUB>3</SUB> itself-elicited inward current was blocked by GABA<SUB>A</SUB> receptor antagonist. The present results indicate that Rg<SUB>3</SUB>-induced GABA<SUB>A</SUB> receptor activation via the γ<SUB>2</SUB> subunit and I<SUB>GABA</SUB> enhancement by Rg<SUB>3</SUB> might be one of the molecular bases of ginseng effects on GABA<SUB>A</SUB> receptor.

Pulchellamin G, an amino acid-sesquiterpene lactone, from Saussurea pulchella suppresses lipopolysaccharide-induced inflammatory responses via heme oxygenase-1 expression in murine peritoneal macrophages

Lee, D.S.,Choi, H.G.,Wan Woo, K.,Kang, D.G.,Lee, H.S.,Oh, H.,Ro Lee, K.,Kim, Y.C. North-Holland ; Elsevier Science Ltd 2013 european journal of pharmacology Vol.715 No.1

Saussurea pulchella (Asteraceae) is widely distributed in Korea and has been used in Korean folk medicine for the treatment of inflammation, hypertension, hepatitis, and arthritis. Pulchellamin G is an amino acid-sesquiterpene lactone conjugate isolated from S. pulchella. In the present study, we focused on the anti-inflammatory effect of pulchellamin G, which acts by inducing the expression of heme oxygenase (HO)-1. HO-1 plays important roles in cytoprotection since it has antioxidant, anti-inflammatory, antiproliferative, and antiapoptotic properties. Pulchellamin G inhibited the mRNA and protein expression of inducible nitric oxide synthase (iNOS), iNOS-derived nitric oxide (NO), and cyclooxygenase (COX)-2 and COX-derived prostaglandin E2 (PGE<SUB>2</SUB>) production in lipopolysaccharide (LPS)-stimulated murine peritoneal macrophages. The compound also reduced tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β) production and suppressed the phosphorylation and degradation of IκB-α and nuclear translocation of p65 in murine peritoneal macrophages in response to LPS stimulus. The inhibitory effects of pulchellamin G on nuclear factor kappa B (NF-κB) translocation was impaired by co-treatment of the cells with HO activity inhibitor tin protoporphyrin (SnPP). By using SnPP, we verified that the inhibitory effects of pulchellamin G on the pro-inflammatory mediators NO, PGE<SUB>2</SUB>, TNF-α, and IL-1β are associated with induction of HO-1 expression. Our data suggest that pulchellamin G might have potent therapeutic effects and it should be considered in the development of treatments for various inflammatory diseases.