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Lee, Ha-Reum,Yoo, Nina,Jeong, Jinseon,Sohn, Ki-Young,Yoon, Sun Young,Kim, Jae Wha Pergamon Press 2018 Thrombosis research Vol.161 No.-
<P><B>Abstract</B></P> <P>Previously, PLAG (1-palmitoyl-2-linoleoyl-3-acetyl-rac-glycerol, acetylated diglyceride) was reported to have an effect on the proliferation of hematopoietic stem cells (HSCs) or to contribute to the prevention of chemotherapy-induced neutropenia. In this study, we examined the role of PLAG in the differentiation of bone marrow cells from HSCs into progenitor cells in mice. After 15days, the lineage-negative cells, especially megakaryocyte/erythrocyte progenitors (MEP), were significantly increased in mice that received daily PLAG administration compared to those in the untreated mice. Furthermore, we explored the possibility that the PLAG-induced increase in MEP will contribute to reduction of chemotherapy-induced thrombocytopenia (CIT) in a thrombocytopenia mouse model. Mice were administrated 5-fluorouracil (5-FU) and PLAG. After 7days, bone marrow cells were analyzed. Treatment with 5-FU powerfully decreased myeloid precursor populations and treatment with 5-FU/PLAG resulted in reduction of decreased myeloid progenitor cell numbers. In addition, numbers of circulating platelets were also increased by PLAG treatment. Taken together, PLAG plays a role in differentiating HSCs toward MEP and alleviating chemotherapy-induced bone marrow cell reduction. Thus PLAG shows its potential to augment the therapeutic effect of anti-cancer drugs-induced thrombocytopenia.</P> <P><B>Highlights</B></P> <P> <UL> <LI> PLAG administration increases the circulating platelet through stimulating differentiation of HSCs toward MEP. </LI> <LI> 5-FU-induced MEP decrease was significantly alleviated following PLAG administration. </LI> <LI> PLAG decreased chemotherapy-induced bone marrow damage and elevated circulating platelet. </LI> </UL> </P>
참당귀의 흰쥐 4-Vessel Occlusion 전뇌허혈에 대한 신경방어효과
김영옥,하니나,부영민,박선영,박주영,유영법,신준식,안덕균,김호철 대한본초학회 2002 大韓本草學會誌 Vol.17 No.2
Objectives : Angelicae Radix, the root of Angelica gigas N_AKAI (Umbelliferae) , which has been used to nourish the blood(補血), regulate menstruation(調經), relieve pain and promote bowel movements(崩漏) and activate blood circulation for the treatment of fatigue, headache, constipation and blood troubles in traditional Korean medicine. It's flavour and channel tropism is sweet(甘), pungent(辛), warm(溫), acting on the lung, heart and spleen(肺, 心, 脾). The purpose of study we report here was to determine the neuroprotective effect of Angelica gigas on global ischemia induced by 4-vessel occlusion in Wistar rats. Methods : Angelica gigas extracts was lyphilized after extraction with 85% methanol. We induced 4-VO for 10 minutes and reperfused again. The number of CA1 pyramidal neurons were counted after 7 days of reperfusion under the cresyl violet staining. Results : The results showed that Angelica gigas had significantly neuroprotective effects (100, 250 and 500mg/kg of AR extracts, p<0.001) compared with control group. Each neuroprotective ratio was about 66.1, 79.3 and 78.6% respectively. Immunohistochemical data partially explained the protective effects of Angelica gigas via attenuation of COX-2 induction in hippocampus. Conclusion : Angelica gigas gas neuroprotective effects on the global ischemia induced by 4-vessel occlusion in Wistar rats and the attenuation of COX-2 induction is thought to be its possible mechanism.
Lee, Dae-Hee,Ha, Nina,Bu, Yung-Min,Choi, Hyoung Il,Park, Yoo Guen,Kim, Yoon Bum,Kim, Mi-Yeon,Kim, Hocheol Pharmaceutical Society of Japan 2006 BIOLOGICAL & PHARMACEUTICAL BULLETIN Vol.29 No.8
<P>The flower buds of <I>Buddleja officinalis</I> M<SMALL>AXIM</SMALL> (Loganiaceae) are used to treat headache and inflammatory diseases in traditional Korean medicine. In the present study, the neuroprotective effects of the methanolic extract of <I>B. officinalis</I> (BOME) and of its hexane fraction (BOHF) were investigated in a middle cerebral artery occlusion (MCAo, 120 min occlusion, 24 h reperfusion) Sprague–Dawley rat model. BOME or BOHF (100 mg/kg, <I>p.o.</I>) was twice administered 30 min before the onset of MCAo and 2 h after reperfusion. BOME and BOHF treated groups showed infarct volumes reduced by 33.9% and 68.2%, respectively, at 2 h occlusion. In BOHF treated animals, cyclooxygenase-2 and iNOS inductions were inhibited in ischemic hemispheres at both the mRNA and protein levels. Furthermore, <I>in vitro</I> studies showed that BOME and BOHF both inhibited LPS-induced nitric oxide production in BV-2 mouse microglial cells. These results suggest that the anti-inflammatory and the microglial activation inhibitory effects of <I>B. officinalis</I> extract may contribute to its neuroprotective effects in brain ischemia.</P>
Oh, Sehyun,Oh, Hyun Woo,Lee, Ha‐,Reum,Yoon, Sun Young,Oh, Sei‐,Ryang,Ko, Young‐,Eun,Yoo, Nina,Jeong, Jinseon,Kim, Jae Wha John Wiley Sons, Ltd 2016 Journal of the science of food and agriculture Vol.96 No.8
<P>BACKGROUND: Euphorbia kansui, a traditional medical herb, has been shown to have anti-tumour and anti-viral activities. Previously, we have reported that E. kansui increases interferon-gamma (IFN-gamma) production in natural killer (NK) cells. However, it is not clear how E. kansui regulates IFN-gamma secretion by NK cells. RESULTS: In this study, E. kansui was separated into six individual compounds from the same chloroform fraction so that the activity of each compound could be compared. E. kansui compounds induced IFN-gamma secretion through the phosphorylation of protein kinase D and I kappa B kinase pathways. Furthermore, E. kansui compounds activated the translocation of p65, a sub-unit of nuclear factor kappa-light-chain-enhancer of activated B cells (NF-kappa B), to the nucleus and induced NF-kappa B at the transcriptional level. CONCLUSION: These findings suggest that E. kansui enhances IFN-gamma secretion through the NF-kappa B pathway in NK cells. (c) 2015 Society of Chemical Industry</P>
Siberian ginseng reduces infarct volume in transient focal cerebral ischaemia in Sprague-Dawley rats
Bu, Yungmin,Jin, Zhen Hua,Park, Sun Young,Baek, Sunkyung,Rho, Sungju,Ha, Nina,Park, Seong Kyu,, Sun Yeo Kim,Kim, Hocheol John Wiley Sons, Ltd. 2005 Phytotherapy research Vol.19 No.2
<P>Siberian ginseng, the root and stem bark of Acanthopanax senticosus Harms, has been used as a tonic and adaptogen to strengthen qi in traditional Korean medicine. The neuroprotective effects of water extracts of A. senticosus (ASW) were investigated in transient middle cerebral artery occlusion (MCAo, 90 min occlusion, 24 h reperfusion) of Sprague-Dawley rats. The infarct volume was significantly reduced by 36.6% after the peritoneal injection of ASW (100 mg[sol ]kg) compared with the control. In the immunohistochemical study, ASW markedly inhibited both cyclooxygenase-2 and OX-42 expressions in the penumbral region at 24 h after MCAo. These results suggest that A. senticosus has a neuroprotective effect by inhibiting inflammation and microglial activation in brain ischaemia. Copyright © 2005 John Wiley & Sons, Ltd.</P>
Jae-Hwan Park,Dal-hyun Kim,In-Chang Hwang,Nina Ha,Sera Lee,Jung Min Kim,Sung Sook Lee,Hosung Yu,In-Taek Lim,Jun-A You 대한약학회 2011 Archives of Pharmacal Research Vol.34 No.3
CKD-712 is a 1-naphthyl analog of higenamine that has been reported to have potent antiinflammatory and thus anti-sepsis effects. The purpose of this study was to investigate the potential of CKD-712 as a medicine for sepsis and to confirm its protective effects on organs in animal sepsis models. Pretreatment with CKD-712 dose-dependently increased survival rate in a lipopolysaccharide-induced sepsis model in mice. Body temperature decrease, an important pre-symptom of septic death, was also prevented by CKD-712. CKD-712 still significantly increased survival rate even when administered one and four hours after lipopolysaccharide injection. Therapeutic efficacy of CKD-712 was also confirmed against sepsis following zymosan-induced endotoxemia and in cecal ligation and puncture surgery in mice. In a disseminated intravascular coagulation model in rats, CKD-712 showed organ-protective effect by reducing serum glutamate-oxaloacetate transaminase, glutamate-pyruvate transferase, blood urea nitrogen, and creatinine levels. CKD-712 also prevented histological damage to the lung and liver. In this same model, CKD-712 showed anti-inflammatory effects through decreases in tumor necrosis factor-α and interleukin-6 in the blood and reduced translocation of nuclear factor-κB to the nuclei of lung cells. CKD-712 administration also diminished infiltration of leukocytes into the lung and liver. Taken together, these results show that CKD-712 has excellent potential as an effective medicine for sepsis.
Oh, Bo Ram,Suh, Dong-hyeon,Bae, Daekwon,Ha, Nina,Choi, Young Il,Yoo, Hyun Jung,Park, Jin Kyun,Lee, Eun Young,Lee, Eun Bong,Song, Yeong Wook BioMed Central 2017 Arthritis research & therapy Vol.19 No.-
<P><B>Background</B></P><P>Histone deacetylase (HDAC) inhibitor has recently been reported to have a therapeutic effect as an anti-inflammatory agent in collagen-induced arthritis (CIA). We investigated the therapeutic effect of a new selective HDAC6 inhibitor, CKD-L, compared to ITF 2357 or Tubastatin A on CIA and regulatory T (Treg) cells in patients with rheumatoid arthritis (RA).</P><P><B>Methods</B></P><P>CIA was induced by bovine type II collagen (CII) in DBA/1 J mice. Mice were treated with HDAC inhibitor for 18 days. Arthritis score was assessed and histological analysis was performed by hematoxylin and eosin (H&E) stain. Cytotoxic T-lymphocyte associated protein (CTLA)-4 expression in induced Treg cells was analyzed and suppression assay was analyzed using Treg cells and effector T (Teff) cells isolated from naive C57BL/6 mice by flow cytometry. Cytokines were analyzed in peripheral blood mononuclear cells (PBMC) of five patients with RA by enzyme-linked immunosorbent assay (ELISA) and real-time polymerase chain reaction (PCR). Tumor necrosis factor (TNF) was analyzed using PMA- activated THP-1 cells by ELISA. Suppression assay was analyzed using Treg cells and Teff cells isolated from RA patients by flow cytometry.</P><P><B>Results</B></P><P>In the CIA model, CKD-L and Tubastatin A significantly decreased the arthritis score. CKD-L increased CTLA-4 expression in Foxp3<SUP>+</SUP> T cells and inhibited the proliferation of Teff cells in the suppression assay. In RA PBMC, CKD-L significantly inhibited TNF and interleukin (IL)-1β, and increased IL-10. CKD-L and Tubastatin A inhibited TNF secretion from PMA-activated THP-1 cells. CKD-L and ITF 2357 inhibited the proliferation of Teff cells in RA patients in the suppression assay. Tubastatin A had no effect on inhibition of proliferation.</P><P><B>Conclusion</B></P><P>CKD-L decreased the arthritis score in CIA, reduced the expression of TNF and IL-1β, and increased the expression of IL-10 in PBMC from RA patients. CKD-L increased CTLA-4 expression and the suppressive function of Treg cells. These results suggest that CKD-L may have a beneficial effect in the treatment of RA.</P>
Endan Li,Jiwoo Choi,Hye-Ri Sim,Jiyeon Kim,Jae Hyun Jun,Jangbeen Kyung,Nina Ha,Keun Ho Ryu,Seung Soo Chung,Hyun Sook Kim,Semi Kim,Sungsu Lee,Wongi Seol,송지환 생화학분자생물학회 2023 BMB Reports Vol.56 No.3
Huntington’s disease (HD) is a neurodegenerative disorder, ofwhich pathogenesis is caused by a polyglutamine expansion inthe amino-terminus of huntingtin gene that resulted in the aggregationof mutant HTT proteins. HD is characterized by progressivemotor dysfunction, cognitive impairment and neuropsychiatricdisturbances. Histone deacetylase 6 (HDAC6), amicrotubule-associated deacetylase, has been shown to inducetransport- and release-defect phenotypes in HD models, whilsttreatment with HDAC6 inhibitors ameliorates the phenotypiceffects of HD by increasing the levels of α-tubulin acetylation,as well as decreasing the accumulation of mutant huntingtin(mHTT) aggregates, suggesting HDAC6 inhibitor as a HD therapeutics. In this study, we employed in vitro neural stem cell(NSC) model and in vivo YAC128 transgenic (TG) mouse modelof HD to test the effect of a novel HDAC6 selective inhibitor,CKD-504, developed by Chong Kun Dang (CKD PharmaceuticalCorp., Korea). We found that treatment of CKD-504 increasedtubulin acetylation, microtubule stabilization, axonaltransport, and the decrease of mutant huntingtin protein invitro. From in vivo study, we observed CKD-504 improved thepathology of Huntington’s disease: alleviated behavioral deficits,increased axonal transport and number of neurons, restoredsynaptic function in corticostriatal (CS) circuit, reduced mHTTaccumulation, inflammation and tau hyperphosphorylation inYAC128 TG mouse model. These novel results highlight CKD-504as a potential therapeutic strategy in HD.