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Abstract Background Sagunja-Tang (SGT-4) is a traditional herbal formula in Korean medicine that is used to treat anti-metabolic syndrome, and has antioxidant activity. In this study, we evaluated the effects of SGT-4 on the formation efficiency of induced pluripotent stem cells (iPSCs) from human foreskin fibroblasts (HFFs) by four reprogramming transcription factors: Oct4, Sox2, KIf4, and c-Myc (OSKM). Methods SGT-4 contained four different herbal medicines that are composed of Ginseng Radix, Glycyrrhizae Radix et Rhizoma, Atractylodis Rhizoma Alba, and Poria Sclerotium. The composition of SGT-4 was analyzed by high-performance liquid chromatography (HPLC). HFFs were transfected with episomal vectors contained by four OSKM. Western blotting, RT-PCR, immunofluroescence, and in vitro differentiation were used to assess the pluripotency of the iPSC cells. Results SGT-4 exhibited antioxidant activity against the generation of intracellular reactive oxygen species (ROS) as well as promoted the activation of superoxide dismutase 1 (SOD1), catalase, gluthathione peroxidase 1 (GPX1), and glutathione (GSH). Moreover, the ATP level was not significantly fluctuated depending on the concentration of SGT-4 in the hiPSCs. Conclusion Our results indicate that the SGT-4, herbal formula significantly increases the efficiency of human iPSC generation via the transcription factors (Oct4, Sox2, KIf4, and c-Myc).

An outbreak of nosocomial infections with Middle East respiratory syndrome coronavirus occurred in South Korea in May 2015. Spike glycoprotein genes of virus strains from South Korea were closely related to those of strains from Riyadh, Saudi Arabia. However, virus strains from South Korea showed strain-specific variations.

In May 2015, Middle East respiratory syndrome coronavirus infection was laboratory confirmed in South Korea. Patients were a man who had visited the Middle East, his wife, and a man who shared a hospital room with the index patient. Rapid laboratory confirmation will facilitate subsequent prevention and control for imported cases.

Sulforaphane (1-isothiocyanato-4-(methylsulfinyl)-butane), belongingto a family of natural compounds that are abundant in broccoli,has received significant therapeutic interest in recent years.However, the molecular basis of its effects remains to beelucidated. In this study, we attempt to determine whether sulforaphaneregulates the inflammatory response in an ovalbumin(OVA)-induced murine asthma model. Mice were sensitizedwith OVA, treated with sulforaphane, and then challenged withOVA. Sulforaphane administration significantly alleviated theOVA-induced airway hyperresponsiveness to inhaled methacholine.Additionally, sulforaphane suppressed the increase inthe levels of SOCS-3 and GATA-3 and IL-4 expression in theOVA-challenged mice. Collectively, our results demonstrate thatsulforaphane regulates Th2 immune responses. This sutdy providesnovel insights into the regulatory role of sulforaphane in allergen-induced Th2 inflammation and airway responses, whichindicates its therapeutic potential for asthma and other allergicdiseases. [BMB reports 2012; 45(5): 311-316]

In asthma, T helper 2 (TH2)-type cytokines such as interleukin(IL)-4, IL-5, and IL-13 are produced by activated CD4+ T cells.Dendritic cells played an important role in determining thefate of naïve T cells into either TH1 or TH2 cells. Wedetermined whether RG-II regulates the TH1/TH2 immuneresponse by using an ovalbumin-induced murine model ofasthma. RG-II reduced IL-4 production but increased interferon-gamma production, and inhibited GATA-3 geneexpression. RG-II also inhibited asthmatic reactions includingan increase in the number of eosinophils in bronchoalveolarlavage fluid, an increase in inflammatory cell infiltration inlung tissues, airway luminal narrowing, and airway hyperresponsiveness.This study provides evidence that RG-II plays acritical role in ameliorating the pathogenic process ofasthmatic inflammation in mice. These findings provide newinsights into the immunotherapeutic role of RG-II in terms ofits effects in a murine model of asthma. [BMB reports 2012;45(2): 79-84]

The downstream of kinase (DOK)-1 is involved in the protein tyrosine kinase (PTK) pathway in mast cells, but the role of DOK-1 in the pathogenesis of asthma has not been defined. In this study, we have demonstrated a novel regulatory role of DOK-1 in airway inflammation and physiologic responses in a murine model of asthma using lentiviral vector containing DOK-1 cDNA or DOK-1-specific ShRNA. The OVA-induced inflammatory cells, airway hyperresponsiveness, Th2 cytokine expression, and mucus response were significantly reduced in DOK-1 overexpressing mice compared to OVA-challenged control mice. The transgenic introduction of DOK-1 significantly stimulated the activation and expression of STAT-4 and T-bet, while impressively inhibiting the activation and expression of STAT-6 and GATA-3 in airway epithelial cells. On the other hand, DOK-1 knockdown mice enhanced STAT-6 expression and its nuclear translocation compared to OVA-challenged control mice. When viewed in combination, our studies demonstrate DOK-1 regulates allergen-induced Th2 immune responses by selective stimulation and inhibition of STAT-4 and STAT-6 signaling pathways, respectively. These studies provide a novel insight on the regulatory role of DOK-1 in allergen-induced Th2 inflammation and airway responses, which has therapeutic potential for asthma and other allergic diseases.