Chang D S, Seo S J, Hong C K
Department of Dermatology, Yongsan Hospital, Chung Ang University School of Medicine, Seoul, Korea.
Photodermatol Photoimmunol Photomed. 2002 Dec;18(6):280-6. doi: 10.1034/j.1600-0781.2002.02752.x.
BACKGROUND/PURPOSE: Amniotic membrane (AM) is the innermost fetal membrane, which contains several proteinase inhibitors and expresses several growth factors. Nitric oxide (NO) has been implicated in the pathogenesis of various inflammatory diseases including sunburn and ultraviolet induced erythema. The expression of inducible nitric oxide synthase (iNOS) is up regulated by UVB irradiation and inhibited by TGF-beta and EGF-beta. We evaluated the effect of AM extract on the expression of iNOS mRNA by UV irradiation in HaCaT cell (immortalized human keratinocyte cell line).
HaCaT cells were irradiated UVB 30 mJ/cm2 and AM extract was added. The iNOS mRNA was isolated by RT-PCR and NO production was assessed by spectrophotometric method based on Griess reaction.
The expression of iNOS mRNA was induced by UVB irradiation in HaCaT cell and the expression of iNOS mRNA was higher at 48 h than that at 24 h. AM extract down regulated the induction of iNOS mRNA in HaCaT cell by UVB irradiation. NO generation was increased by UVB irradiation, but down regulated by AM extract treatment in HaCaT cells.
These results assured that the expression of iNOS mRNA and generation of NO are up regulated by UVB irradiation and showed that AM extract down regulated the induction of iNOS mRNA and decreased generation of NO by UVB irradiation.
背景/目的:羊膜是最内层的胎膜,含有多种蛋白酶抑制剂并表达多种生长因子。一氧化氮(NO)与包括晒伤和紫外线诱导的红斑在内的各种炎症性疾病的发病机制有关。诱导型一氧化氮合酶(iNOS)的表达受紫外线B(UVB)照射上调,并受转化生长因子-β(TGF-β)和表皮生长因子-β(EGF-β)抑制。我们评估了羊膜提取物对UVB照射下人永生化角质形成细胞系(HaCaT细胞)中iNOS mRNA表达的影响。
用30 mJ/cm2的UVB照射HaCaT细胞并添加羊膜提取物。通过逆转录聚合酶链反应(RT-PCR)分离iNOS mRNA,并基于格里斯反应通过分光光度法评估NO的产生。
UVB照射诱导HaCaT细胞中iNOS mRNA的表达,且iNOS mRNA在48小时时的表达高于24小时时的表达。羊膜提取物下调UVB照射诱导的HaCaT细胞中iNOS mRNA的表达。UVB照射增加HaCaT细胞中NO的生成,但羊膜提取物处理可下调其生成。
这些结果证实UVB照射上调iNOS mRNA的表达和NO的生成,并表明羊膜提取物下调UVB照射诱导的iNOS mRNA表达并减少NO的生成。