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Choi, Eun Hye,Ok, Hyun Ee,Yoon, Yoosik,Magnuson, Bernadene A.,Kim, Mi Kyung,Chun, Hyang Sook John Wiley & Sons, Inc. 2007 Biofactors Vol.29 No.1
<P>The toxicities associated with 5-fluorouracil (5-FU), a potent broad-spectrum chemotherapeutic agent, can not only affect the morbidity and the efficacy of chemotherapy but also limit its clinical use. The objective of this study is to investigate the effects of a commercial anthocyanin-rich extract from bilberry (AREB) against 5-FU-induced myelotoxicity in vivo, and against chemosensitivity to 5-FU in vitro. A single injection of 5-FU at 200 mg/kg induced severe peripheral erythrocytopenia, thrombocytopenia and leucopenia as well as hypocellularity of the spleen and bone marrow in C57BL/6 mice. Oral administration of 500 mg/kg of AREB for 10 days significantly increased the number of red blood cells, neutrophils, and monocytes in peripheral blood to 1.2-fold, 9-fold, and 6-fold, respectively, compared with those seen after treatment with 5-FU alone (p< 0.05–0.001). The hypocellularity of the spleen and bone marrow caused by 5-FU was also distinctly alleviated in the AREB-treated group. Furthermore, AREB treatment with 50 and 100 μg/ml as a monomeric anthocyanin did not interfere with, but rather enhanced the chemotherapeutic efficacy of 5-FU in vitro. These results suggest that AREB may have protective potential against 5-FU-induced myelotoxiciy and/or the ability to enhance the chemotherapeutic effectiveness of 5-FU.</P>
Critical role for arginase II in osteoarthritis pathogenesis
Choi, Wan-Su,Yang, Jeong-In,Kim, Wihak,Kim, Hyo-Eun,Kim, Seul-Ki,Won, Yoonkyung,Son, Young-Ok,Chun, Churl-Hong,Chun, Jang-Soo BMJ Publishing Group Ltd 2019 Annals of the Rheumatic Diseases Vol.78 No.3
<P><B>Objective</B></P><P>Osteoarthritis (OA) appears to be associated with various metabolic disorders, but the potential contribution of amino acid metabolism to OA pathogenesis has not been clearly elucidated. Here, we explored whether alterations in the amino acid metabolism of chondrocytes could regulate OA pathogenesis.</P><P><B>Methods</B></P><P>Expression profiles of amino acid metabolism-regulating genes in primary-culture passage 0 mouse chondrocytes were examined by microarray analysis, and selected genes were further characterised in mouse OA chondrocytes and OA cartilage of human and mouse models. Experimental OA in mice was induced by destabilisation of the medial meniscus (DMM) or intra-articular (IA) injection of adenoviruses expressing catabolic regulators. The functional consequences of arginase II (Arg-II) were examined in <I>Arg2<SUP>−/−</SUP> </I> mice and those subjected to IA injection of an adenovirus encoding Arg-II (Ad-Arg-II).</P><P><B>Results</B></P><P>The gene encoding Arg-II, an arginine-metabolising enzyme, was specifically upregulated in chondrocytes under various pathological conditions and in OA cartilage from human patients with OA and various mouse models. Adenovirus-mediated overexpression of Arg-II in mouse joint tissues caused OA pathogenesis, whereas genetic ablation of <I>Arg2</I> in mice (<I>Arg2</I> <SUP>−/−</SUP>) abolished all manifestations of DMM-induced OA. Mechanistically, Arg-II appears to cause OA cartilage destruction at least partly by upregulating the expression of matrix-degrading enzymes (matrix metalloproteinase 3 [MMP3] and MMP13) in chondrocytes via the nuclear factor (NF)-κB pathway.</P><P><B>Conclusions</B></P><P>Our results indicate that Arg-II is a crucial regulator of OA pathogenesis in mice. Although chondrocytes of human and mouse do not identically, but similarly, respond to Arg-II, our results suggest that Arg-II could be a therapeutic target of OA pathogenesis.</P>
( Eun Ae Jo ),( Su Keong Jung ),( Jung Hoon Lee ),( Jeong Ok Kim ),( Heaong Eun Choi ),( Hae Sun Joo ),( Hoa Yeon Choi ),( Shin A Jang ),( Sung Ook Hwang ),( Soo Ran Choi ) 대한주산의학회 2018 Perinatology Vol.29 No.2
Amniotic Fluid Embolism: Maternal Disseminated Intravascular Coagulation, Cardiovascular Collapse, and Acute Hypoxic Cases Shortly after Delivery