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RISS 인기검색어
- 검색키워드
- 저자 : Gumy, Fré (검색결과 2 건)
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Sensitized near-IR luminescence of lanthanide complexes based on push-pull diketone derivatives
Baek, Nam Seob,Kim, Yong Hee,Eom, Yu Kyung,Oh, Jung Hwan,Kim, Hwan Kyu,Aebischer, Annina,Gumy, Fré,dé,ric,Chauvin, Anne-Sophie,Bü,nzli, Jean-Claude G. Royal Society of Chemistry 2010 Dalton Transactions Vol.39 No.6
<P>Lanthanide complexes with two push-pull diketone derivatives as sensitizers have been developed as synthons for near-infrared emitting materials. The ligand substituents consist of a carbazole moiety with hole-transport properties and an aromatic or heteroaromatic unit. According to quantitative NMR analysis and complementary HPLC experiments, the diketones are predominantly in their enolic form in polar solvents such as THF and MeCN at room temperature. The preferred <I>cis</I>-enol form contributes strongly to the binding of lanthanide ions (Ln = Nd, Gd, Er). The resulting tris(diketonate) ternary complexes with terpyridine (Ln = Nd, Er) display sizeable near-IR emission with long luminescence lifetimes.</P> <P>Graphic Abstract</P><P>Lanthanide complexes with two push-pull diketone derivatives as sensitizers have been developed as synthons for near-infrared emitting materials. <IMG SRC='http://pubs.rsc.org/services/images/RSCpubs.ePlatform.Service.FreeContent.ImageService.svc/ImageService/image/GA?id=b915893f'> </P>
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Gu, M. Y.,Kim, J.,Yang, H. O. Springer Science + Business Media 2016 Neurochem Res Vol.41 No.6
<P>Justicidin A is a structurally defined arylnaphthalide lignan, which has been shown anti-cancer activity; however, the neuroprotective effect of justicidin A is still untested. In this study, we investigated the action of justicidin A on amyloid beta (A beta)(25-35)-induced neuronal cell death via inhibition of the hyperphosphorylation of tau and induction of autophagy in SH-SY5Y cells. Pretreatment with justicidin A significantly elevated cell viability in cells treated with A beta(25-35). Western blot data demonstrated that justicidin A inhibited the A beta(25-35)-induced up-regulation the levels of hyperphosphorylation of tau in SH-SY5Y cells. In addition, treatment with justicidin A significantly induced autophagy as measured by the increasing LC3 II/I ratio, an important autophagy marker. These studies showed that justicidin A inhibited activity of glycogen synthase kinase-3beta (GSK-3 beta), which is an important kinase in up-stream signaling pathways; inhibited hyperphosphorylation of tau in AD; and enhanced activity of AMP-activated protein kinase (AMPK), which is the key molecule for both hyperphosphorylation of tau and induction of autophagy. These data provide the first evidence that justicidin A protects SH-SY5Y cells from A beta(25-35)-induced neuronal cell death through inhibition of hyperphosphorylation of tau and induction of autophagy via regulation the activity of GSK-3 beta and AMPK, and they also provide some insights into the relationship between tau protein hyperphosphorylation and autophagy. Thus, we conclude that justicidin A may have a potential role for neuroprotection and, therefore, may be used as a therapeutic agent for AD.</P>
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