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LIGHT enhances the bactericidal activity of human monocytes and neutrophils via HVEM
Heo, Sook-Kyoung,Ju, Seong-A,Lee, Sang-Chul,Park, Sang-Min,Choe, Suck-Young,Kwon, Byungsuk,Kwon, Byoung S.,Kim, Byung-Sam Wiley (John WileySons) 2006 Journal of Leukocyte Biology Vol.79 No.2
<P>Human monocytes and neutrophils play major roles in clearing bacteria from human blood and tissues. We found that the herpes virus entry mediator (HVEM) was highly expressed in monocytes and neutrophils, and its interaction with 'homologous to lymphotoxins, shows inducible expression, and competes with herpes simplex virus glycoprotein D for HVEM/tumor necrosis factor (TNF)-related 2' (LIGHT) enhanced bactericidal activity against Listeria monocytogenes and Staphylococcus aureus. The LIGHT-HVEM interaction increased levels of phagocytosis, interleukin (IL)-8, TNF-alpha, nitric oxide (NO), and reactive oxygen species (ROS) in monocytes and neutrophils. Anti-HVEM monoclonal antibody was able to block LIGHT-induced bactericidal activity, cytokine production (IL-8 and TNF-alpha), and ROS generation. Moreover, inhibition of ROS and NO production blocked LIGHT-induced bactericidal activity. Our results indicate that the LIGHT/HVEM interaction in monocytes and neutrophils contributes to antibacterial activity.</P>
Rhein augments ATRA-induced differentiation of acute promyelocytic leukemia cells
Heo, Sook-Kyoung,Noh, Eui-Kyu,Kim, Jeong Yi,Jegal, SungHoo,Jeong, Yookyung,Cheon, Jaekyung,Koh, SuJin,Baek, Jin Ho,Min, Young Joo,Choi, Yunsuk,Jo, Jae-Cheol Elsevier 2018 Phytomedicine Vol.49 No.-
<P><B>Abstract</B></P> <P><B>Background</B></P> <P>Rhein (4, 5-dihydroxyanthraquinone-2-carboxylic acid), a natural anthraquinone derivative, is a traditional Chinese herb that has been used as a medication in many Asian countries. It has been used as a laxative and stomach drug for a long time in both China and Korea. It is well-known to have many pharmacological activities, such as anti-cancer, anti-bacterial, anti-fungal, anti-oxidant, anti-atherogenic, anti-angiogenic, anti-fibrosis, anti-inflammatory, hepatoprotective, and nephroprotective properties. However, little is known about how rhein may affect the differentiation activities in acute promyelocytic leukemia (APL) cells.</P> <P><B>Purpose</B></P> <P>The present study was designed to examine the anti-leukemic effects of rhein against APL cells and to explore the underlying mechanism.</P> <P><B>Methods</B></P> <P>Cell viability was investigated by MTS assay. To examine the differentiation activities in APL cells, the cell surface molecules (CD11b, CD14, CCR1 and CCR2), phagocytosis, reactive oxygen species (ROS) were determined by flow cytometry. Also, induction of caspase-3 activity and reduction of mitochondrial membrane potential (MMP) were determined by flow cytometry. RNA and protein expressions were determined by qRT-PCR and western blotting, respectively.</P> <P><B>Results</B></P> <P>In this study we assessed the role of rhein in treating APL. Interestingly, rhein potentiated all-trans retinoic acid (ATRA)-induced macrophage differentiation in NB4 cells by inducing changes in morphology, expression of the differentiation markers CD11b and CD14, ROS production, phagocytic activity, and expression of CCR1 and CCR2. Signaling through CD11b was found to be dependent on ERK activation. Additionally, rhein induced APL cell death by activating apoptosis and suppressing the mTOR pathway.</P> <P><B>Conclusion</B></P> <P>Therefore, we suggest that a combination of rhein and ATRA carries strong therapeutic potential through the beneficial differentiation of APL cells. Moreover, rhein causes cell death via the activation of apoptosis and suppression of survival signals in APL cells. In combination with the ability of rhein to promote functional macrophage differentiation in APL, these properties suggest that a combined treatment of rhein and ATRA has great potential as an anti-leukemic therapy for APL.</P> <P><B>Graphical abstract</B></P> <P>[DISPLAY OMISSION]</P>
Evodiamine and rutaecarpine inhibit migration by LIGHT via suppression of NADPH oxidase activation
Heo, Sook-Kyoung,Yun, Hyun-Jeong,Yi, Hyo-Seung,Noh, Eui-Kyu,Park, Sun-Dong Wiley Subscription Services, Inc., A Wiley Company 2009 Journal of cellular biochemistry Vol.107 No.1
<P>LIGHT acted as a new player in the atherogenesis. The dried, unripe fruit of Evodia Fructus (EF) has long been used as a traditional Chinese herbal medicine, and is currently widely used for the treatment of headache, abdominal pain, vomiting, colds and reduced blood circulation. Evodiamine and rutaecarpine are active components of EF. In this study, we investigated the inhibitory effect of evodiamine and rutaecarpine on LIGHT-induced migration in human monocytes. Evodiamine and rutaecarpine decreased the LIGHT-induced production of ROS, IL-8, monocyte chemoattractant protein-1 (MCP-1), TNF-α, and IL-6, as well as the expression of chemokine receptor (CCR) 1, CCR2 and ICAM-1 and the phosphorylation of the ERK 1/2 and p38 MAPK. Furthermore, NADPH oxidase assembly inhibitor, AEBSF, blocked LIGHT-induced migration and activation of CCR1, CCR2, ICAM-1, and MAPK such as ERK and p38 in a manner similar to evodiamine and rutaecarpine. These findings indicate that the inhibitory effects of evodiamine and rutaecarpine on LIGHT-induced migration and the activation of CCR1, CCR2, ICAM-1, ERK, and p38 MAPK occurs via decreased ROS production and NADPH oxidase activation. Taken together, these results indicate that evodiamine and rutaecarpine have the potential for use as an anti-atherosclerosis agent. J. Cell. Biochem. 107: 123–133, 2009. © 2009 Wiley-Liss, Inc.</P>
Heo, Sook‐,Kyoung,Yun, Hyun‐,Jeong,Park, Won‐,Hwan,Park, Sun‐,Dong Wiley Subscription Services, Inc., A Wiley Company 2008 Journal of cellular biochemistry Vol.105 No.1
<P><B>Abstract</B></P><P>Vascular smooth‐muscle cell (VSMC) proliferation plays a vital role in hypertension, atherosclerosis and restenosis. It has been reported that emodin, an active component extracted from rhubarb, can stop the growth of cancer cells; however, it is not known if emodin exerts similar anti‐atherogenic effects in TNF‐α treated human aortic smooth‐muscle cells (HASMC). In this study, emodin treatment showed potent inhibitory effects in TNF‐α‐induced HASMC proliferation that were associated with induced apoptosis, including the cleavage of poly ADP‐ribose polymerase (PARP). Moreover, inhibitors of caspase‐3, ‐8 and ‐9 (Ac‐DEVD‐CHO, Z‐IETD‐FMK and Z‐LEHD‐FMK) efficiently blocked emodin‐induced apoptosis in TNF‐α treated HASMC. Therefore, emodin‐induced cell death occurred via caspase‐dependent apoptosis. Emodin treatment resulted in the release of cytochrome <I>c</I> into cytosol and a loss of mitochondrial membrane potential (ΔΨ<SUB>m</SUB>), as well as a decrease in the expression of an anti‐apoptotic protein (Bcl‐2) and an increase in the expression of an a pro‐apoptotic protein (Bax). Emodin‐mediated apoptosis was also blocked by a mitochondrial membrane depolarization inhibitor, which indicates that emodin‐induced apoptosis occurred via a mitochondrial pathway. Taken together, the results of this study showed that emodin inhibits TNF‐α‐induced HASMC proliferation via caspase‐ and a mitochondrial‐dependent apoptotic pathway. In addition, these results indicate that emodin has potential as an anti‐atherosclerosis agent. J. Cell. Biochem. 105: 70–80, 2008. © 2008 Wiley‐Liss, Inc.</P>
Heo Eunjeong,Choi Yoonhee,Kim Hyung-sook,Namgung Hyung Wook,Lee Eunsook,Lee Euni,Lee Ju-Yeun,Jung Jongtak,Kim Eu Suk,Kim Hong Bin,Song Kyoung-Ho 대한감염학회 2023 Infection and Chemotherapy Vol.55 No.2
Background: Systematic protocols for the management of outpatient parenteral antimicrobial therapy (OPAT) and information on the current status of a prescription of parenteral antibiotics for outpatients and referred patients are lacking in the Korea. This study aimed to describe the current status of OPAT at a tertiary care hospital in Korea. Materials and Methods: This was a retrospective study of outpatients and referral patients who were prescribed parenteral antibiotics from July to December 2019. We reviewed the prescribed antimicrobials, indications for antimicrobial therapy, institution administering the antimicrobial injections, and pre- and post-prescription management. Results: Of the 577 prescriptions assessed in this study, 399 (69.2%) and 178 (30.8%) were delivered using the referral and outpatient models, respectively. About 70% of OPATs were prescribed in the pulmonology, infectious diseases, orthopedics, gastroenterology, and hematology departments. Five antibiotics (ertapenem [26.0%], ceftriaxone [12.8%], kanamycin [11.8%], amikacin [10.1%], and cefazolin [8.5%]) accounted for 69.2% of the total OPATs. Urinary tract (27.3%), respiratory (20.8%), and intra-abdominal (15.9%) infections were the most frequent indications for OPAT. After prescription, there were 295 (73.9%) and 150 (84.3%) follow-up visits in the referral and outpatient models, respectively (P <0.05). Laboratory tests necessary for monitoring were fully performed for 274 (47.5%) prescriptions. Conclusion: We found that a significant number of OPATs were prescribed, follow-up visits were not performed in the case of about a quarter of prescriptions, and laboratory monitoring was not fully conducted in more than half of the cases. Therefore, it is necessary to establish an appropriate management program for OPAT. Considering the limited resources and the distribution of OPAT prescriptions, an effective strategy may be to select the frequently-used antibiotics or frequently-prescribing departments and start the program with them.
Effect of KIOM-79 against mitochondrial damage induced by streptozotocin in pancreatic beta-cells.
Kang, Kyoung Ah,Kim, Jin Sook,Zhang, Rui,Piao, Mei Jing,Ko, Dong Ok,Wang, Zhi Hong,Heo, Young Jun,Park, Doek Bae,Maeng, Young Hee,Hyun, Jin Won Taylor Francis 2009 Journal of toxicology and environmental health. Pa Vol.72 No.20
<P>The present study examined the effects of KIOM-79 on streptozotocin (STZ)-induced mitochondrial oxidative stress in rat pancreatic beta-cells (RINm5F). KIOM-79 is a mixture of plant extracts from parched Puerariae radix, gingered Magnoliae cortex, Glycyrrhizae radix, and Euphorbiae radix. A marked increase in mitochondrial reactive oxygen species (ROS) was observed in STZ induced diabetic cells, which returned to control conditions after KIOM-79 treatment. Mitochondrial manganese superoxide dismutase (Mn SOD) activity and its protein expression were downregulated by STZ treatment but upregulated by KIOM-79 treatment. In addition, KIOM-79 treatment restored the loss of the mitochondrial membrane potential (Deltapsi) produced by STZ treatment. KIOM-79 induced an increase in Bcl-2 and a decrease in phospho Bcl-2 and Bax, which are related to permeability of the mitochondrial membrane. Further, KIOM-79 inhibited the translocation of cytochrome c from the mitochondria to the cytosol and elevated the ATP level, which was reduced by STZ treatment. These results suggest that KIOM-79 exhibits a protective effect through activation of antioxidant defense mechanisms and by attenuation of mitochondrial dysfunction in STZ-induced diabetic cells.</P>