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- 저자 : Wu Guiying (검색결과 2 건)
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Wu Huiying,Wu Guiying,Yao Ping,Zhou Yan,Zhang Feng,Zuo Baoqi 한국고분자학회 2018 폴리머 Vol.42 No.5
In this work, silk fibroin (SF) filament with fibrils regenerated by dissolving in CaCl₂-formic acid (FA) was prepared by wet-spun method at room temperature. Different from traditional dissolved methods, SF solutions obtained by dissolving in CaCl₂-FA preserved fibrils, which have been recognized as the key to the high performance of native silk. The morphology of SF filament was analyzed, very dense filaments with smooth surface and circular, nanofibrils could be observed in longitudinal and cross-sections of filaments. Moreover, the breaking stress of samples was gradually increased with the increase of draw-down ratios. After 3 times drawing, the breaking stress and elongation at break of filament were 276.4±22.6 MPa and 40.8±3.1%, respectively. At the same time, the secondary structure of SF filament was typical β-sheet. In addition, SF filaments showed excellent degradation property, the mass lost of SF filament declined 42% after incubating in protease XIV solution. Above all, the human mesenchymal stem cells (hMSCs) adhered very well on the surface of the filaments, which demonstrated the good biocompatibility of SF filaments, was suitable for application in tissue engineering.
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Li, Guiying,Han, Chang,Xu, Lihong,Lim, Kyu,Isse, Kumiko,Wu, Tong Wiley Subscription Services, Inc., A Wiley Company 2009 Hepatology Vol.50 No.3
<P><B>Abstract</B></P><P>Cyclooxygenase‐2 (COX‐2)–derived prostaglandins participate in a number of pathophysiological responses such as inflammation, carcinogenesis, and modulation of cell growth and survival. This study used complementary approaches of COX‐2 transgenic (Tg) and knockout (KO) mouse models to evaluate the mechanism of COX‐2 in Fas‐induced hepatocyte apoptosis and liver failure <I>in vivo</I>. We generated Tg mice with targeted expression of COX‐2 in the liver by using the albumin promoter‐enhancer–driven vector. The COX‐2 Tg, COX‐2 KO, and wild‐type mice were treated with the anti‐Fas antibody Jo2 (0.5 μg/g of body weight) for 4 to 6 hours, and the extent of liver injury was assessed by histopathology, serum aminotransferases, TUNEL staining, and caspase activation. The COX‐2 Tg mice showed resistance to Fas‐induced liver injury in comparison with the wild‐type mice; this was reflected by the lower alanine aminotransferase (ALT) and aspartate aminotransferase (AST) levels, less liver damage, and less hepatocyte apoptosis (<I>P</I> < 0.01). In contrast, the COX‐2 KO mice showed significantly higher serum ALT and AST levels, more prominent hepatocyte apoptosis, and higher levels of caspase‐8, caspase‐9, and caspase‐3 activity than the wild‐type mice (<I>P</I> < 0.01). The COX‐2 Tg livers expressed higher levels of epidermal growth factor receptor (EGFR) than the wild‐type controls; the COX‐2 KO livers expressed the lowest levels of EGFR. Pretreatment with a COX‐2 inhibitor (NS‐398) or an EGFR inhibitor (AG1478) exacerbated Jo2‐mediated liver injury and hepatocyte apoptosis. <I>Conclusion:</I> These findings demonstrate that COX‐2 prevents Fas‐induced hepatocyte apoptosis and liver failure at least in part through up‐regulation of EGFR. (H<SMALL>EPATOLOGY</SMALL> 2009.)</P>
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