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Vitamin D_(3)가 RAW 세포에 감염된 Mycobacterium marinum의 증식억제에 미치는 기전 연구
박정규,정샛별,이길수,김수영,송창화,박종호,조현구,조은경,김화중 충남대학교 의과대학 의학연구소 2003 충남의대잡지 Vol.30 No.1
The natural resistance-associated macrophage protein 1(Nramp1) has been proposed to directly regulate bactericidal or bacteriostatic activity of the macrophage toward pathogens or participate in macrophage activation that lead to microbial elimination in the host. The relationship between Nramp1 and nitric oxide(NO) as an antimicrobial factor has not been precisely defined to date. To devise an in vitro assay for Nramp1 function, this study introduced a wild type Nramp1^(G169) cDKA transfected RAW264.7 macrophages(A8) which bear a homozygous mutant Nramp1^(D169) allele and are permissive to replication of specific intracellular parasites. RAW264.7 and A8 macrophages did not produce NO, but vitamin D_(3)-activated-Mycobacterium marinum-infected RAW264.7 and A8 macrophages pretreated with vitamin D_(3) leaded to the increase of NO production and growth inhibition of M. marinum. Inhibition of NO production by a NO inhibitor, L-NAME, abolished the above effects. The mRNA expression of iNOS in infected macrophages with costimulated vitamin D_(3) was increased. IFN-γ activated macrophages also showed the same results with vitamin D_(3) activated macrophages. These results suggest that bactericidal or bacteriostatic activity in RAW264.7 and A8 macrophages correlated with the production of NO, although NO might not be the only factor responsible for controlling M. marinum infection. The Nrampl gene is considered to be a cofactor in the controlling the replication of M. marinum infection.
Rg3-enriched Korean Red Ginseng improves vascular function in spontaneously hypertensive rats
Jung-Bum Park,Sun Kwan Kwon,Harsha Nagar,Saet-byel Jung,Byeong Hwa Jeon,Chang Sup Kim,Jin-Hwan Oh,Hee-Jung Song,Cuk-Seong Kim 고려인삼학회 2014 Journal of Ginseng Research Vol.38 No.4
Background: Panax ginseng has distinct and impressive health benefits, such as improved blood pressure and immune system functioning. Rg3-enriched Korean Red Ginseng (REKRG) isolated from Korean Red Ginseng contains a high percentage of Rg3. Methods: In this study, we examined the effects of REKRG on endothelial cell nitric oxide synthase (eNOS) activation and adhesion molecules in endothelial cells and vascular function in rats. Results: REKRG dose-dependently increased eNOS phosphorylation and nitric oxide (NO) production in endothelial cells. In addition, REKRG markedly inhibited the tumor necrosis factor-a (TNF-α)-mediated induction of intercellular adhesion molecule (ICAM)-1 and cyclooxygenase (COX)-2 expressions in endothelial cells. REKRG improved endothelium-dependent vasorelaxation in the Wistar-Kyoto (WKY) rat and spontaneously hypertensive rats (SHRs) compared with controls. Furthermore, REKRG treatment for 6 weeks increased serum NO levels and reduced the mean aortic intima-media thickness compared with controls. Conclusion: Taken together, these results suggest that REKRG increased vascular function and improved immune system functioning. Therefore, REKRG is a very useful food for preventing or improving various cardiovascular diseases.
Jung, Saet-Byel,Yang, Chul-Su,Lee, Ji-Sook,Shin, A-Rum,Jung, Sung-Soo,Son, Ji Woong,Harding, Clifford V.,Kim, Hwa-Jung,Park, Jeong-Kyu,Paik, Tae-Hyun,Song, Chang-Hwa,Jo, Eun-Kyeong American Society for Microbiology 2006 Infection and immunity Vol.74 No.5
<B>ABSTRACT</B><P>Although the 38-kDa glycolipoprotein of <I>Mycobacterium tuberculosis</I> H37Rv is known to evoke prominent cellular and humoral immune responses in human tuberculosis (TB), little information is known about intracellular regulatory mechanisms involved in 38-kDa antigen (Ag)-induced host responses. In this study, we found that purified 38-kDa glycolipoprotein activates mitogen-activated protein kinases (MAPKs; extracellular signal-regulated kinase 1/2 [ERK1/2] and p38) and induces tumor necrosis factor alpha (TNF-α) and interleukin 6 (IL-6) in human monocytes. When the 38-kDa Ag was applied to monocytes from TB patients and healthy controls, the activation of ERK1/2 and p38 MAPK and the subsequent cytokine secretion were greater in the monocytes from the active pulmonary TB patients than in monocytes from the healthy controls. Additionally, neutralizing antibodies for Toll-like receptor 2 (TLR2) or TLR4 significantly reduced the ERK1/2 and p38 activation induced by the 38-kDa protein when the antibodies were applied to HEK293 cells overexpressing TLR2 or TLR4 as well as human primary monocytes. Furthermore, the inhibition of TLR2 significantly, and that of TLR4 partially, decreased the 38-kDa Ag-induced secretion of TNF-α and IL-6 in human monocytes. The intact protein moieties of the 38-kDa protein were responsible for biologic activities by this Ag. These data collectively demonstrate that the 38-kDa glycolipoprotein, acting through both TLR2 and TLR4, induces the activation of the ERK1/2 and p38 MAPK pathways, which in turn play an essential role in TNF-α and IL-6 expression during mycobacterial infection.</P>
결핵균 튜베르쿨린 PPD 및 38-kDa 항원에 의한 사람 말초혈액 단핵구의 전염증성 사이토카인 생성에 대한 Toll-like Receptor 의존도 비교 분석
정샛별(Saet-Byel Jung),이지숙(Ji-Sook Lee),양철수(Chul-Su Yang),송창화(Chang-Hwa Song),이길수(Kil-Soo Lee),김화중(Hwa-Jung Kim),박정규(Jeong-Kyu Park),백태현(Tae-Hyun Paik),조은경(Eun-Kyeong Jo) 대한미생물학회 2007 Journal of Bacteriology and Virology Vol.37 No.1
Rg3-enriched Korean Red Ginseng improves vascular function in spontaneously hypertensive rats
Park, Jung-Bum,Kwon, Sun Kwan,Nagar, Harsha,Jung, Saet-Byel,Jeon, Byeong Hwa,Kim, Chang Sup,Oh, Jin-Hwan,Song, Hee-Jung,Kim, Cuk-Seong The Korean Society of Ginseng 2014 Journal of Ginseng Research Vol.38 No.4
Background: Panax ginseng has distinct and impressive health benefits, such as improved blood pressure and immune system functioning. Rg3-enriched Korean Red Ginseng (REKRG) isolated from Korean Red Ginseng contains a high percentage of Rg3. Methods: In this study, we examined the effects of REKRG on endothelial cell nitric oxide synthase (eNOS) activation and adhesion molecules in endothelial cells and vascular function in rats. Results: REKRG dose-dependently increased eNOS phosphorylation and nitric oxide (NO) production in endothelial cells. In addition, REKRG markedly inhibited the tumor necrosis factor-${\alpha}$ (TNF-${\alpha}$)-mediated induction of intercellular adhesion molecule (ICAM)-1 and cyclooxygenase (COX)-2 expressions in endothelial cells. REKRG improved endothelium-dependent vasorelaxation in the Wistar-Kyoto (WKY) rat and spontaneously hypertensive rats (SHRs) compared with controls. Furthermore, REKRG treatment for 6 weeks increased serum NO levels and reduced the mean aortic intima-media thickness compared with controls. Conclusion: Taken together, these results suggest that REKRG increased vascular function and improved immune system functioning. Therefore, REKRG is a very useful food for preventing or improving various cardiovascular diseases.
Nagar, Harsha,Jung, Saet-byel,Ryu, Min Jeong,Choi, Su-Jung,Piao, Shuyu,Song, Hee-Jung,Kang, Shin Kwang,Shin, Nara,Kim, Dong Woon,Jin, Seon-Ah,Jeong, Jin-Ok,Irani, Kaikobad,Jeon, Byeong Hwa,Shong, Minh Mary Ann Liebert, Inc. Publishers 2017 Antioxidants & Redox Signaling Vol. No.
<P>Conclusion: These findings indicate that CRIF1 plays an important role in maintaining mitochondrial and endothelial function through its effects on the SIRT1-eNOS pathway.</P>
Min-Woong Kang,Hee-Jung Song,Shin Kwang Kang,Yonghwan Kim,Saet-byel Jung,Sungju Jee,Jae Young Moon,Kwang-sun Suh,Sang Do Lee,Byeong Hwa Jeon,Cuk-Seong Kim 대한생리학회-대한약리학회 2015 The Korean Journal of Physiology & Pharmacology Vol.19 No.3
Nafamostat mesilate (NM) is a serine protease inhibitor with anticoagulant and anti-inflammatory effects. NM has been used in Asia for anticoagulation during extracorporeal circulation in patients undergoing continuous renal replacement therapy and extra corporeal membrane oxygenation. Oxidative stress is an independent risk factor for atherosclerotic vascular disease and is associated with vascular endothelial function. We investigated whether NM could inhibit endothelial dysfunction induced by tumor necrosis factor-α (TNF-α). Human umbilical vein endothelial cells (HUVECs) were treated with TNF-α for 24 h. The effects of NM on monocyte adhesion, vascular cell adhesion molecule-1 (VCAM-1) and intracellular adhesion molecule-1 (ICAM-1) protein expression, p38 mitogenactivated protein kinase (MAPK) activation, and intracellular superoxide production were then examined. NM (0.01∼100 μg/mL) did not affect HUVEC viability; however, it inhibited the increases in reactive oxygen species (ROS) production and p66shc expression elicited by TNF-α (3 ng/mL), and it dose dependently prevented the TNF-α-induced upregulation of endothelial VCAM-1 and ICAM-1. In addition, it mitigated TNF-α-induced p38 MAPK phosphorylation and the adhesion of U937 monocytes. These data suggest that NM mitigates TNF-α-induced monocyte adhesion and the expression of endothelial cell adhesion molecules, and that the anti-adhesive effect of NM is mediated through the inhibition of p66shc, ROS production, and p38 MAPK activation.
P53 Impairs Endothelium-Dependent Vasomotor Function Through Transcriptional Upregulation of P66shc
Kim, Cuk-Seong,Jung, Saet-Byel,Naqvi, Asma,Hoffman, Timothy A.,DeRicco, Jeremy,Yamamori, Tohru,Cole, Marsha P.,Jeon, Byeong-Hwa,Irani, Kaikobad Ovid Technologies Wolters Kluwer -American Heart A 2008 Circulation research Vol.103 No.12
<P>The transcription factor, p53, and the adaptor protein, p66shc, both play essential roles in promoting oxidative stress in the vascular system. However, the relationship between the two in the context of endothelium-dependent vascular tone is unknown. Here, we report a novel, evolutionarily conserved, p53-mediated transcriptional mechanism that regulates p66shc expression and identify p53 as an important determinant of endothelium-dependent vasomotor function. We provide evidence of a p53 response element in the promoter of p66shc and show that angiotensin II-induced upregulation of p66shc in endothelial cells is dependent on p53. In addition, we demonstrate that downregulation of p66shc expression, as well as inhibition of p53 function in mice, mitigates angiotensin II-induced impairment of endothelium-dependent vasorelaxation, decrease in bioavailable nitric oxide, and hypertension. These findings reveal a novel p53-dependent transcriptional mechanism for the regulation of p66shc expression that is operative in the vascular endothelium and suggest that this mechanism is important in impairing endothelium-dependent vascular relaxation.</P>
Nafamostat mesilate promotes endothelium-dependent vasorelaxation via the Akt-eNOS dependent pathway
Choi, Sujeong,Kwon, Hyon-Jo,Song, Hee-Jung,Choi, Si Wan,Nagar, Harsha,Piao, Shuyu,Jung, Saet-byel,Jeon, Byeong Hwa,Kim, Dong Woon,Kim, Cuk-Seong The Korean Society of Pharmacology 2016 The Korean Journal of Physiology & Pharmacology Vol.20 No.5
Nafamostat mesilate (NM), a synthetic serine protease inhibitor, has anticoagulant and anti-inflammatory properties. The intracellular mediator and external anti-inflammatory external signal in the vascular wall have been reported to protect endothelial cells, in part due to nitric oxide (NO) production. This study was designed to examine whether NM exhibit endothelium dependent vascular relaxation through Akt/endothelial nitric oxide synthase (eNOS) activation and generation of NO. NM enhanced Akt/eNOS phosphorylation and NO production in a dose- and time-dependent manner in human umbilical vein endothelial cells (HUVECs) and aorta tissues obtained from rats treated with various concentrations of NM. NM concomitantly decreased arginase activity, which could increase the available arginine substrate for NO production. Moreover, we investigated whether NM increased NO bioavailability and decreased aortic relaxation response to an eNOS inhibitor in the aorta. These results suggest that NM increases NO generation via the Akt/eNOS signaling pathway, leading to endothelium-dependent vascular relaxation. Therefore, the vasorelaxing action of NM may contribute to the regulation of cardiovascular function.