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  • 學位論文

羥基紅花黃素A在UVA誘導光損傷下對人類皮膚角質細胞之影響

The effects of hydroxysafflor yellow A (HSYA) on UVA-induced damage in HaCaT keratinocytes

指導教授 : 簡怡雯

摘要


紫外線 (ultraviolet light, UV) 的曝曬是一個潛在性的環境危害,過量曝曬會引起許多急性或慢性的皮膚損傷。造成皮膚光損傷主要是接觸紫外線的照射而引起細胞內活性氧物質的生成,提升細胞內的氧化壓力而誘發DNA的損傷以及細胞膜脂質過氧化,促進發炎反應並干擾細胞的代謝途徑。紅花,學名Carthamus tinctorius L.為傳統的藥用植物,富含黃酮類 (flavonoids),羥基紅花黃素A (hydroxysafflor yellow A, HSYA) 為主要的活性成分。近年研究指出HSYA可透過清除自由基並改善氧化壓力傷害而被認為具有抗氧化、抗凝血、抗發炎等功用,不過並未在皮膚保健的領域作相關探討,故本研究的目的在探討羥基紅花黃素A (HSYA)在細胞模式中對於光損傷的影響。實驗方法:事先給予HaCaT皮膚角質細胞羥基紅花黃素A培養24小時,在予以照射能量200 mJ/cm2的UVA,探討細胞內的ROS和MDA的生成以評估氧化壓力,並測量MMP-1, MMP-2, MMP-9以及促發炎因子COX-2的mRNA表現量。結果顯示給予HSYA的介入可以明顯提高細胞存活率,減少氧化自由基與脂質過氧化物MDA的生成,並可藉由降低氧化壓力來降低細胞內基質金屬蛋白酶MMP-1, MMP-2, MMP-9以及促發炎反應因子COX-2的mRNA表現量來達到細胞於光損傷下的保護作用。因此,羥基紅花黃素A對於UVA所引起的光損傷具有保護效果。

並列摘要


UV radiation from sunlight cause numbers of acute and chronic skin damage which can result in inflammation, immune changes, physical changes and DNA damage that facilitates skin aging and the development of skin carcinogenesis. Reactive oxygen species (ROS) are generated by excessive solar UV radiation, resulting in oxidative damage to cellular components, proteins, lipids, and nucleic acids. Thus, antioxidation plays an important role to protect skin against ROS-induced injury. Safflower (Carthamus tinctorius L.) is an important Chinese medicine containing abundant flavones and hydroxysafflor yellow A (HSYA) which is its main active ingredient. HSYA is a part of quinochalcone and has unique structures of hydroxy groups that provide an antioxidant effect. In this study, the aim was to investigate the protective role of HSYA in human keratinocytes (HaCaT) against UVA-induced oxidative damage and the possible mechanism. The HaCaT cells were UVA-irradiated and the effects of HSYA on cell viability, reactive oxygen species generation, lipid peroxidation and mRNA expression were measured. The mRNA expression of matrix metalloproteinase 1 (MMP-1), matrix metalloproteinase 2 (MMP-2), matrix metalloproteinase 9 (MMP-9), cyclooxygenase-2 (COX-2) were determined by RT-PCR. In this study, UVA exposure led to a decrease in cell viability and an increase in reactive oxygen species generation in HaCaT cells. HSYA could effectively increase the viability of HaCaT cells after UVA exposure and protect them from UVA-induced oxidative stress. Moreover, HSYA inhibited the expression of MMP-1, MMP-2, MMP-9 and COX-2 in UVA-induced photodamaged HaCaT cells. Our results suggest that HSYA can act as a free radical scavenger while keratinocytes are photodamaged. HSYA has potential as a skin protective ingredient against UVA-induced photodamage.

參考文獻


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