Skin photoaging is a complex, multifactorial process resulting in functional and structural changes of the skin, and different phenotypes from chronological skin aging are well-recognized. Ultraviolet (UV)-irradiated ...Skin photoaging is a complex, multifactorial process resulting in functional and structural changes of the skin, and different phenotypes from chronological skin aging are well-recognized. Ultraviolet (UV)-irradiated hairless mice have been used as a skin photoaging animal model. However, differences in morphology and gene expression patterns between UV-induced and chronological skin changes in this mouse model have not been fully elucidated. Here we investigated differences in histopathology and cytokine expression between UV-irradiated and non-irradiated aged hairless mice to clarify the factor(s) that differentiate photoaging from chronological skin aging phenotypes. Eight-week-old HR-1 hairless mice were divided into UV-irradiated (UV-irradiated mice) and non-irradiated (control mice) groups. Irradiation was performed three times per week for 10 weeks. In addition, 30-week-old HR-1 hairless mice were reared until 70 weeks of age without UV irradiation (aged mice). Histopathologies revealed that the flattening of dermal-epidermal junctions and epidermal thickening were observed only in UV-irradiated mice. Decreases in fine elastic fibers just beneath the epidermis, the thickening of elastic fibers in the reticular dermis, and the accumulation of glycosaminoglycans were more prominent in UV-irradiated mice as compared to non-irradiated aged mice. Quantitative PCR analyses revealed that UV-irradiated mice showed an increase in the expression of IFN-γ. In contrast, aged mice exhibited proportional up-regulation of both pro-inflammatory and anti-inflammatory cytokines. The IFN-γ/IL-4 ratio, an indicator for the balance of pro-inflammatory and anti-inflammatory cytokines, was significantly higher in UV-irradiated mice as compared to control and non-irradiated aged mice. An elevated IFN-γ/IL-4 ratio was also observed in aged senescence-accelerated mouse-prone 1 (SAMP1) mice, a spontaneous skin photoaging model we recently reported. Thus, an imbalance between pro-inflammatory and anti-inflammatory cytokines might be a key factor to differentiate photoaged skin from chronologically-aged skin.展开更多
目的:确定SKH-1无毛小鼠光老化模型的造模方法,并将该模型用于点阵CO_(2)激光治疗效应观察。方法:将15只SKH-1无毛小鼠分为空白组、较低剂量紫外线组和较高剂量紫外线组,紫外线照射小鼠背部皮肤,通过观察小鼠背部皮肤外观、HE染色评估...目的:确定SKH-1无毛小鼠光老化模型的造模方法,并将该模型用于点阵CO_(2)激光治疗效应观察。方法:将15只SKH-1无毛小鼠分为空白组、较低剂量紫外线组和较高剂量紫外线组,紫外线照射小鼠背部皮肤,通过观察小鼠背部皮肤外观、HE染色评估小鼠皮肤光老化程度,选定合适的紫外线照射剂量。10只光老化小鼠随机分为对照组与点阵CO_(2)激光治疗组,治疗前、治疗后即刻、7d、14d及28d检测经皮水分丢失(Trans-epidermal water loss,TEWL),治疗前、治疗后即刻、28d、56d行环钻活检取得皮肤组织,进行HE染色、Masson染色、阿新蓝染色及Ⅰ型、Ⅲ型胶原免疫组化染色。结果:紫外线照射后SKH-1小鼠背部皮肤出现皮肤粗糙,横向皱纹增加,胶原纤维含量显著减少、疏松、断裂,真皮变薄、表皮增厚等光老化表现,紫外线剂量过高可出现日光性角化甚至癌变。点阵CO_(2)激光治疗即刻皮肤组织内可形成锥形的微小热损伤区,TEWL即刻显著升高7倍,1~2周恢复,逐渐出现胶原新生。结论:SKH-1无毛小鼠是较理想的光老化动物实验模型,且可用于点阵激光等美容治疗后的生理与组织学研究。展开更多
文摘Skin photoaging is a complex, multifactorial process resulting in functional and structural changes of the skin, and different phenotypes from chronological skin aging are well-recognized. Ultraviolet (UV)-irradiated hairless mice have been used as a skin photoaging animal model. However, differences in morphology and gene expression patterns between UV-induced and chronological skin changes in this mouse model have not been fully elucidated. Here we investigated differences in histopathology and cytokine expression between UV-irradiated and non-irradiated aged hairless mice to clarify the factor(s) that differentiate photoaging from chronological skin aging phenotypes. Eight-week-old HR-1 hairless mice were divided into UV-irradiated (UV-irradiated mice) and non-irradiated (control mice) groups. Irradiation was performed three times per week for 10 weeks. In addition, 30-week-old HR-1 hairless mice were reared until 70 weeks of age without UV irradiation (aged mice). Histopathologies revealed that the flattening of dermal-epidermal junctions and epidermal thickening were observed only in UV-irradiated mice. Decreases in fine elastic fibers just beneath the epidermis, the thickening of elastic fibers in the reticular dermis, and the accumulation of glycosaminoglycans were more prominent in UV-irradiated mice as compared to non-irradiated aged mice. Quantitative PCR analyses revealed that UV-irradiated mice showed an increase in the expression of IFN-γ. In contrast, aged mice exhibited proportional up-regulation of both pro-inflammatory and anti-inflammatory cytokines. The IFN-γ/IL-4 ratio, an indicator for the balance of pro-inflammatory and anti-inflammatory cytokines, was significantly higher in UV-irradiated mice as compared to control and non-irradiated aged mice. An elevated IFN-γ/IL-4 ratio was also observed in aged senescence-accelerated mouse-prone 1 (SAMP1) mice, a spontaneous skin photoaging model we recently reported. Thus, an imbalance between pro-inflammatory and anti-inflammatory cytokines might be a key factor to differentiate photoaged skin from chronologically-aged skin.
文摘目的:确定SKH-1无毛小鼠光老化模型的造模方法,并将该模型用于点阵CO_(2)激光治疗效应观察。方法:将15只SKH-1无毛小鼠分为空白组、较低剂量紫外线组和较高剂量紫外线组,紫外线照射小鼠背部皮肤,通过观察小鼠背部皮肤外观、HE染色评估小鼠皮肤光老化程度,选定合适的紫外线照射剂量。10只光老化小鼠随机分为对照组与点阵CO_(2)激光治疗组,治疗前、治疗后即刻、7d、14d及28d检测经皮水分丢失(Trans-epidermal water loss,TEWL),治疗前、治疗后即刻、28d、56d行环钻活检取得皮肤组织,进行HE染色、Masson染色、阿新蓝染色及Ⅰ型、Ⅲ型胶原免疫组化染色。结果:紫外线照射后SKH-1小鼠背部皮肤出现皮肤粗糙,横向皱纹增加,胶原纤维含量显著减少、疏松、断裂,真皮变薄、表皮增厚等光老化表现,紫外线剂量过高可出现日光性角化甚至癌变。点阵CO_(2)激光治疗即刻皮肤组织内可形成锥形的微小热损伤区,TEWL即刻显著升高7倍,1~2周恢复,逐渐出现胶原新生。结论:SKH-1无毛小鼠是较理想的光老化动物实验模型,且可用于点阵激光等美容治疗后的生理与组织学研究。
