http://chineseinput.net/에서 pinyin(병음)방식으로 중국어를 변환할 수 있습니다.
변환된 중국어를 복사하여 사용하시면 됩니다.
Bae, Han-Sol,Yoon, Won-Joon,Cho, Young-Dan,Islam, Rabia,Shin, Hye-Rim,Kim, Bong-Soo,Lim, Jin-Muk,Seo, Min-Seok,Cho, Seo-Ae,Choi, Kang-Young,Baek, Seung-Hak,Kim, Hong-Gee,Woo, Kyung-Mi,Baek, Jeong-Hwa Wiley (John WileySons) 2017 Journal of Bone and Mineral Research Vol. No.
<P>Cleidocranial dysplasia (CCD) is an autosomal dominant skeletal disorder caused by mutations in RUNX2, coding a key transcription factor of early osteogenesis. CCD patients suffer from developmental defects in cranial bones. Despite numerous investigations and clinical approaches, no therapeutic strategy has been suggested to prevent CCD. Here, we show that fetal administration of Entinostat/MS-275, a class I histone deacetylase (HDAC)-specific inhibitor, partially prevents delayed closure of cranial sutures in Runx2(+/-) mice strain of C57BL/6J by two mechanisms: 1) posttranslational acetylation of Runx2 protein, which stabilized the protein and activated its transcriptional activity; and 2) epigenetic regulation of Runx2 and other bone marker genes. Moreover, we show that MS-275 stimulates osteoblast proliferation effectively both in vivo and in vitro, suggesting that delayed skeletal development in CCD is closely related to the decreased number of progenitor cells as well as the delayed osteogenic differentiation. These findings provide the potential benefits of the therapeutic strategy using MS-275 to prevent CCD. (c) 2017 American Society for Bone and Mineral Research.</P>
Rehmannia glutinosa suppresses inflammatory responses elicited by advanced glycation end products.
Baek, Gui-Hyun,Jang, Yong-Suk,Jeong, Seung-Il,Cha, Jaeho,Joo, Myungsoo,Shin, Sang-Woo,Ha, Ki-Tae,Jeong, Han-Sol Kluwer Academic/Plenum Publishers 2012 INFLAMMATION Vol.35 No.4
<P>Fresh rhizome of Rehmannia glutinosa Libosch. (Saeng-jihwang in Korean: SJH) has been prescribed for the treatment of diabetes-associated complications. The purpose of the present study is to investigate the underlying mechanisms of the efficacy of SJH in diabetes-related complications. Decoction was obtained after boiling SJH in water and subsequent lyophilization. The cellular toxicity of SJH was determined by MTT assay. The antioxidant activity of SJH was measured by DPPH and DCFH-DA assays. The effects of SJH on inflammatory responses elicited by AGEs were assessed by western blotting and semi-quantitative RT-PCR analyses. The water extract of SJH had a high free radical scavenging activity in vitro and decreased the level of intracellular ROS in THP-1 cells treated with AGEs. SJH suppressed the expression of pro-inflammatory genes, including TNF-α, MCP-1, IP-10, COX-2, and iNOS; the activation of NF-κB; and the expression of RAGE, a receptor for AGEs, where the expressions of which were induced by AGEs. These results suggest the possibility that SJH can be an alternative therapeutics for diabetes-associated diseases.</P>