【摘 要】
：
目的 探讨水通道蛋白3(aquaporin 3,AQP3)、半胱氨酸蛋白酶14(Caspase 14)、博来霉素水解酶(bleomycin hydrolase,BH)在慢性湿疹患者皮肤屏障中的作用以及窄谱中波紫外线(NB
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目的 探讨水通道蛋白3(aquaporin 3,AQP3)、半胱氨酸蛋白酶14(Caspase 14)、博来霉素水解酶(bleomycin hydrolase,BH)在慢性湿疹患者皮肤屏障中的作用以及窄谱中波紫外线(NB-UVB)治疗慢性湿疹的部分作用机制.方法 多功能皮肤测试仪测定30例慢性湿疹患者皮损及非皮损处皮肤含水量及经皮水分丢失(TEWL).免疫组化方法检测AQP3、Caspasel4、BH在慢性湿疹患者皮损及非皮损处的表达.400、800、1200 mJ/cm2三组不同剂量NB-UVB照射培养的角质形成细胞,免疫印迹方法检测AQP3、Caspase14及BH蛋白表达变化.结果 慢性湿疹患者皮损部位皮肤含水量显著减少,约为11.32±5.25,经皮水分丢失明显增加,约为86.28±16.35,与非皮损处比较,差异有统计学意义(P＜0.05).慢性湿疹患者皮损处AQP3及Caspase 14表达显著增高,分别为非皮损处的5.3倍及4.2倍.BH表达显著下降,约为非皮损处的1/3.皮损处与非皮损处比较差异有统计学意义(P＜0.05).400、800、1200 mJ/cm2 NB-UVB照射角质形成细胞后,AOP3及BH蛋白表达均明显下降,分别为对照组的0.48、0.23、0.16;0.82、0.78、0.22.而Caspase 14表达只有在1200 mJ/cm2较高剂量NB-UVB照射后才显著下降,为对照组的0.34.与对照组相比,差异有统计学意义(P＜0.05).结论 慢性湿疹患者皮肤屏障功能受损可能与BH表达减少,Caspase 14及AQP3表达增加有关,NB-UVB治疗慢性湿疹的部分作用机制可能与下调AQP3、Caspasel4及BH的表达有关.
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