中华皮肤科杂志
中華皮膚科雜誌
중화피부과잡지
Chinese Journal of Dermatology
2012年
7期
463-465
,共3页
许雪珠%李雪丽%尚爱民%唐云%大塚藤男
許雪珠%李雪麗%尚愛民%唐雲%大塚籐男
허설주%리설려%상애민%당운%대총등남
紫外线%晒伤%NF-E2相关因子2%活性氧%Keap1
紫外線%曬傷%NF-E2相關因子2%活性氧%Keap1
자외선%쇄상%NF-E2상관인자2%활성양%Keap1
Ultraviolet rays%Sunburn%NF-E2-related factor 2%Reactive oxygen species%Keap1
[目的]观察Nrf2-Keap1通路在保护皮肤免受中波紫外线(UVB)影响中的作用.[方法]8周龄雌性野生型(即Nrf2+/+组)和Nrf2-/-小鼠,每组8只,分别用200 mJ/cm2 UVB(FL120SE灯)照射小鼠耳朵背侧,用刻度计分别测量UVB照射前和照射后1、2、4、7、9、11、14 d小鼠耳朵厚度,记录照射前后两组鼠耳皮肤镜下形态,36 h取各组鼠耳标本进行HE染色及TUNEL实验,记录结果并进行统计学分析.[结果]Nrf2-/-组小鼠耳平均厚度为(0.49±0.22) cm,Nrf2+/+组为(0.25±0.03) cm,经秩和检验,差异有统计学意义(P＜0.01).UVB照射小鼠后36 h组织学检查,Nrf2-/-组真皮水肿和表皮坏死,淋巴细胞浸润和真皮血管扩张更显著；表皮晒伤细胞数[(17.0±3.9)/视野]也较Nrf2+/+组[(5.0±1.7)/视野]明显,两组差异有统计学意义(P＜ 0.01)；Nrf2-/-组TUNEL阳性细胞数约是Nrf2+/+组的5倍.单一UVB照射Nrf2-/-小鼠较Nrf2+/+小鼠发生更强烈而持久的晒伤反应.[结论]Nrf2-Keap1通路可保护皮肤免受UVB的影响,包括由于UVB照射引起的细胞凋亡和氧化损伤.
[目的]觀察Nrf2-Keap1通路在保護皮膚免受中波紫外線(UVB)影響中的作用.[方法]8週齡雌性野生型(即Nrf2+/+組)和Nrf2-/-小鼠,每組8隻,分彆用200 mJ/cm2 UVB(FL120SE燈)照射小鼠耳朵揹側,用刻度計分彆測量UVB照射前和照射後1、2、4、7、9、11、14 d小鼠耳朵厚度,記錄照射前後兩組鼠耳皮膚鏡下形態,36 h取各組鼠耳標本進行HE染色及TUNEL實驗,記錄結果併進行統計學分析.[結果]Nrf2-/-組小鼠耳平均厚度為(0.49±0.22) cm,Nrf2+/+組為(0.25±0.03) cm,經秩和檢驗,差異有統計學意義(P＜0.01).UVB照射小鼠後36 h組織學檢查,Nrf2-/-組真皮水腫和錶皮壞死,淋巴細胞浸潤和真皮血管擴張更顯著；錶皮曬傷細胞數[(17.0±3.9)/視野]也較Nrf2+/+組[(5.0±1.7)/視野]明顯,兩組差異有統計學意義(P＜ 0.01)；Nrf2-/-組TUNEL暘性細胞數約是Nrf2+/+組的5倍.單一UVB照射Nrf2-/-小鼠較Nrf2+/+小鼠髮生更彊烈而持久的曬傷反應.[結論]Nrf2-Keap1通路可保護皮膚免受UVB的影響,包括由于UVB照射引起的細胞凋亡和氧化損傷.
[목적]관찰Nrf2-Keap1통로재보호피부면수중파자외선(UVB)영향중적작용.[방법]8주령자성야생형(즉Nrf2+/+조)화Nrf2-/-소서,매조8지,분별용200 mJ/cm2 UVB(FL120SE등)조사소서이타배측,용각도계분별측량UVB조사전화조사후1、2、4、7、9、11、14 d소서이타후도,기록조사전후량조서이피부경하형태,36 h취각조서이표본진행HE염색급TUNEL실험,기록결과병진행통계학분석.[결과]Nrf2-/-조소서이평균후도위(0.49±0.22) cm,Nrf2+/+조위(0.25±0.03) cm,경질화검험,차이유통계학의의(P＜0.01).UVB조사소서후36 h조직학검사,Nrf2-/-조진피수종화표피배사,림파세포침윤화진피혈관확장경현저；표피쇄상세포수[(17.0±3.9)/시야]야교Nrf2+/+조[(5.0±1.7)/시야]명현,량조차이유통계학의의(P＜ 0.01)；Nrf2-/-조TUNEL양성세포수약시Nrf2+/+조적5배.단일UVB조사Nrf2-/-소서교Nrf2+/+소서발생경강렬이지구적쇄상반응.[결론]Nrf2-Keap1통로가보호피부면수UVB적영향,포괄유우UVB조사인기적세포조망화양화손상.
[Objective] To investigate the roles of Nrf2-Keap1 system in the protection of skin from ultraviolet B (UVB)-induced damage.[Methods] The dorsal surface of ears of 8 wild-type and 8 nrf2-null mutant 8-week-old female mice was exposed to a single dose of UVB irradiation (200 mJ/cm2) by using a FL120SE UV lamp source.Then,the morphology of ears was observed with the measurement of thickness before,as well as on day 1,2,4,7,9,11 and 14 after,the irradiation.Biopsy specimens were taken from the ears 36hours after the irradiation and subjected to hematoxylin and eosin staining as well as terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) assay.The test Results were recorded and statistically analyzed by rank sum test and t test.[Results] A significant increase was observed in the thickness of mouse ears and number of sunburn cells per high-power field (400 ×) in nrf2-null mutant mice compared with wild-type mice ((0.49 ± 0.22) cm vs.(0.25 ± 0.03) cm,P＜ 0.01; 17.0 ± 3.9 vs.5.0 ± 1.7,t=13.8,P＜ 0.01).The number of TUNEL positive cells in the nrf2-null mutant mice was about 5 times that in the wild mice.The sunburn reaction appeared more intense and persistent in nrf2-null mutant mice than in the wild mice.[Conclusion] Nrf2-Keap1 pathway may protect skin against acute UVB damage,including cell apoptosis and oxidative damage.
