Psoriasis is a chronic inflammatory skin disease that affects approximately 2% of worldwide population, and causing long-term troubles to the patients. Therefore, it is urgent to develop safe and effective therapeutic drugs. Catalpol is a natural iridoid glucoside, that has several remarkable pharmacological effects, however, whether catalpol can alleviated psoriasis has not been explored. The goal of the present work is to study the role of catalpol in psoriasis in vivo and in vitro. Imiquimod-induced psoriasislike mice were applied with different concentrations of catalpol for 8 consecutive days. The severity degree of psoriasis was estimated and the skin pathological changes were detected by H&E staining. Also, TNF-α-stimulated keratinocytes were treated with different concentrations of catalpol, then the oxidative stress and inflammation factors, as well as the expression of SIRT1 and activation of NF-kB and MAPK pathways were measured. The results showed that catalpol reduced the erythema, scaling, ear thickness, and changed pathological phenotypes in the lesioned skin region in mice. Treatment with catalpol significantly suppressed the oxidative stress and inflammatory reactions in vivo and in vitro, as reflected by the decreased secretion or expression of oxidative stress indicators and proinflammatory factors. Furthermore, the SIRT1 was up-regulated and the NF-κB and MAPKs signaling pathways were suppressed by the treatment of catalpol in vivo and in vitro. In summary, our data suggested that catalpol may have a therapeutic property of psoriasis by ameliorating oxidative stress and inflammation partly through SIRT1 mediated suppression of NF-κB and MAPKs pathways.
Cimifugin is an important component of chromones in the dry roots of Saposhikovia divaricata for treating inflammatory diseases. However, the possible effect of cimifugin in psoriasis needs further investigation. This current work was designed to evaluate the effects of cimifugin in psoriasis in vivo and in vitro, and unravel the underlying molecular mechanism. Here, we used imiquimod (IMQ) or tumor necrosis factor (TNF)-α to induce a psoriasis-like model in mice or keratinocytes. Obviously, the results showed that cimifugin reduced epidermal hyperplasia, psoriasis area severity index (PASI) scores, ear thickness and histological psoriasiform lesions in IMQ-induced mice. The decreased levels of reduced glutathione (GSH), superoxide dismutase (SOD) and catalase (CAT), and the accumulation of malondialdehyde (MDA) in skin tissues by IMQ were attenuated by cimifugin. Furthermore, it was observed that cimifugin effectively reversed IMQ-induced up-regulation of proinflammatory cytokines, including TNF-α, IL-6, IL-1β, IL-17A, and IL-22. Mechanically, we noticed that cimifugin inhibited IMQ-activated phosphorylation of NF-κB (IκB and p65) and MAPK (JNK, ERK, and p38) signaling pathways. Similar alterations for oxidative stress and inflammation parameters were also detected in TNF-α-treated HaCaT cells. In addition, cimifugin-induced down-regulation of ICAM-1 were observed in TNF-α-treated cells. Altogether, our findings suggest that cimifugin protects against oxidative stress and inflammation in psoriasis-like pathogenesis by inactivating NF-κB/MAPK signaling pathway, which may develop a novel and effective drug for the therapy of psoriasis.
A novel red luminescent material N,N-bis{4-[2-(4-dicyanomethylene-6-methyl-4H-pyran-2yl)ethylene]phenyl}aniline (BDCM) with two (4-dicyanomethylene)-4H-pyran electron-acceptor moieties and a triphenylamine electron-donor moiety for application in organic light-emitting diodes (OLEDs) was synthesized.The resultant compound has a sterically well-hindered structure and a high fluorescence yield. The photoluminescence (PL) of this compound in solution and solid film and the electroluminescence (EL) have been studied. Based on its intense sterically hindered structure, the pure BDCM film prepared shows a bright red PL emission. The three-layered EL device with the structure ITO/CuPc/DPPhP/BDCM/Mg:Ag has a turn-on voltage of less than 4 V, which suggests that BDCM has an excellent electron injection property. A bright luminance of 582 cd m 22 is obtained for the device at 19 V.
A new white-emitting organic diode was realized simply by inserting a doped hole-blocking layer between the hole-transporting layer (HTL) and the electron-transporting layer (ETL). The structure of this device is ITO/CuPc/NPB/blocking layer:rubrene/Alq/MgAg. Copper phthalocyanine (CuPc) was used as a buffer layer; N,N -bis-(1-naphthyl)-N,N -diphenyl-1.1 -biphenyl-4-4 -diamine (NPB) was the HTL; the tris(8-quinolinolato)aluminium complex (Alq) was the ETL; and the trimer of N-arylbenzimidazole (TPBi), 2-(4-biphenylyl-5-(4-tertbutylphenyl)-1,2,3-oxadiazole (PBD) or the 1,2,4-triazole derivative (TAZ) were used as the blocking layers, in which rubrene is doped. The emission spectrum of this device covers a wide range of the visible region and can be sensitively adjusted by the concentration of rubrene. The white emission with CIE (Commission International de l'Eclairage) coordinates x = 0.31, y = 0.32, a maximum luminance of 8635 cd m −2 and maximum luminous efficiency 1.39 lm w −1 (4.9 V) were obtained in the device with a concentration of 1.5% rubrene in TPBi.
A white organic light emitting diode (OLED) has been constructed by employing a new blue material and a red dye directly doped in the blue emitting layer. For comparison, another white cell with a blocking layer has also been made. The configurations of the devices are ITO/CuPc/NPB/JBEM(P):DCJT/Alq/MgAg (device 1) and ITO/CuPc/NPB/TPBi:DCJT/Alq/MgAg (device 2) where copper phthalocyanine (CuPc) is the buffer layer, N,N'-bis-(1-naphthyl)-N,N'-diphenyl-1.1'bipheny1-4-4'-diamine (NPB) is the hole transporting layer, 9,10-bis(3'5'-diaryl)phenyl anthracene doped with perylene (JBEM(P)) is the new blue emitting material, N,arylbenzimidazoles (TPBi) is the hole blocking layer, tris(8-quinolinolato)aluminium complex (Alq) is the electron transporting layer, and DCJT is a red dye. A stable and current independent white OLED has been obtained in device 1, which has a maximum luminance of 14 850 cd m-2, an efficiency of 2.88 Lm W-1, Commission Internationale de l'Eclairage coordinates of x = 0.32, y = 0.38 between 4-200 mA cm-2, and a half lifetime of 2860 h at the starting luminance of 100 cd m-2. Device 1 has a stability more than 50 times better than that of device 2.
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