 |
 |
電話：+86(0)571-87166999
傳真：+86(0)571 86908678
地址：浙江省杭州市江干區(qū)杭海路898-5號(hào)福源鑫大廈
|
|
當(dāng)前位置：首頁(yè) > 國(guó)際交流國(guó)際交流 |
| 文獻(xiàn)摘要：蝦青素，一種葉黃素類型的類胡蘿卜素，在角質(zhì)形成細(xì)胞中抑制紫外線誘導(dǎo)的細(xì)胞凋亡 |
| 發(fā)布時(shí)間：2016/10/8 14:45:00 閱讀次數(shù)：39 |
細(xì)胞內(nèi)的活性氮/氧物種類和細(xì)胞凋亡在紫外誘導(dǎo)的皮膚炎癥反應(yīng)中發(fā)揮重要作用。蝦青素，一種葉黃素類型的類胡蘿卜素，在臨床試驗(yàn)中表現(xiàn)出不同尋常的效果。本文研究了蝦青素對(duì)紫外誘導(dǎo)細(xì)胞凋亡的作用。蝦青素（5 μm）可以導(dǎo)致蛋白含量、誘導(dǎo)性一氧化氮(iNOS)和環(huán)氧合酶(COX)-2的mRNA顯著下降，同時(shí)還可將紫外UVB (20 mJ/cm(2) ) 或UVC (5 mJ/cm(2) )輻射的皮膚表皮角質(zhì)形成細(xì)胞釋放的前列腺素E2降低。在預(yù)先經(jīng)過(guò)蝦青素處理的細(xì)胞中沒有觀察到明顯的紫外誘導(dǎo)的活性氧保護(hù)作用。根據(jù)DNA斷裂分析的證據(jù)顯示，蝦青素可以顯著抑制紫外照射誘導(dǎo)的細(xì)胞凋亡。此外，我們發(fā)現(xiàn)蝦青素處理后可以引起UVB 和 UVC誘導(dǎo)蛋白下降、巨噬細(xì)胞移動(dòng)游走抑制因子mRNA表達(dá)量的下調(diào)以及皮膚表皮角質(zhì)形成細(xì)胞IL-1β 和TNF-α蛋白的下調(diào)。這些結(jié)果表明蝦青素可以有效抑制紫外誘導(dǎo)的炎癥反應(yīng)，減少誘導(dǎo)型一氧化氮（iNOS）的和環(huán)氧合酶的含量，從而抑制皮膚表皮角質(zhì)形成細(xì)胞的凋亡。
Astaxanthin, a xanthophyll carotenoid, inhibits ultraviolet-induced apoptosis in keratinocytesv
Intra-cellular reactive nitrogen/oxygen species and apoptosis play important roles in ultraviolet (UV)-induced inflammatory responses in the skin. Astaxanthin (AST), a xanthophyll carotenoid, exhibits diverse clinical benefits. The protective effects of AST against UV-induced apoptosis were investigated in the present study. Astaxanthin (5 μm) caused a significant decrease in the protein content and the mRNA levels of inducible nitric oxide (iNOS) and cyclooxygenase (COX)-2, and decreased the release of prostaglandin E2 from HaCaT keratinocytes after UVB (20 mJ/cm(2) ) or UVC (5 mJ/cm(2) ) irradiation. No significant protective effects against UV-induced reactive oxygen species (ROS) were observed in AST-pretreated cells. Astaxanthin caused a significant inhibition of UV-irradiation-induced apoptosis, as evidence by a DNA fragmentation assay. Furthermore, we found that the treatment with AST caused a reduction in the UVB- or UVC-induced protein and mRNA expression of macrophage migration inhibitory factor (MIF), IL-1β and TNF-α in HaCaT keratinocytes. These results suggest that AST effectively protects against UV-induced inflammation by decreasing iNOS and COX-2, and thereby inhibiting the apoptosis of keratinocytes.
Exp Dermatol. 2014, 23(3):178-183.
Yoshihisa Y, Rehman MU, Shimizu T.
|
| [返回] |
|
|
