中华皮肤科杂志 ›› 2014, Vol. 47 ›› Issue (12): 899-901.

• 研究报道 • 上一篇    下一篇

表没食子儿茶素没食子酸酯和补骨脂对莫诺苯宗诱导白癜风样小鼠的影响

王翠1,祝逸平2,许爱娥3   

  1. 1. 安徽医科大学附属杭州临床学院
    2. 杭州市第三人民医院
    3. 安徽医科大学附属杭州市第三人民医院皮肤科
  • 收稿日期:2014-03-24 修回日期:2014-09-29 出版日期:2014-12-15 发布日期:2019-06-14
  • 通讯作者: 许爱娥 E-mail:xuaiehz@msn.com
  • 基金资助:
    国家自然科学基金;省部共建计划项目;杭州科技局重大创新项目;浙江省自然科学基金;浙江省自然科学基金

Effect of epigallocatechin gallate and fructus psoraleae on the induction of vitiligo-like depigmentation by monobenzone in mice

Cui WANG1, 1,   

  • Received:2014-03-24 Revised:2014-09-29 Online:2014-12-15 Published:2019-06-14

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摘要： 目的 探讨表没食子儿茶素没食子酸酯（EGCG）和补骨脂对莫诺苯宗诱导的白癜风样小鼠的影响。 方法 C57BL/6小鼠40只，脱去背部2 cm × 2 cm区域毛，随机分为4组，每组10只。阴性对照组涂抹凡士林乳膏；模型组涂抹40%莫诺苯宗乳膏；EGCG组先后涂抹5% EGCG、40%莫诺苯宗乳膏；补骨脂组先后涂抹7%补骨脂、40%莫诺苯宗乳膏。观察小鼠皮肤和毛发脱色情况，组织病理检查观察淋巴细胞浸润，免疫荧光检测CD8+ T细胞表达量。 结果 阴性对照组小鼠皮肤和毛发无脱色现象。模型组小鼠在用药部位及非用药部位均有脱色现象，EGCG组和补骨脂组小鼠用药部位全部出现脱色，用药部位出现脱色斑的平均时间分别为16.7、29.3和19.9 d，脱色面积指数分别为4.00 ± 0.00、2.11 ± 0.54、2.84 ± 0.79，EGCG组、补骨脂组和模型组之间脱色面积指数差异有统计学意义（F = 14.17，P < 0.05），EGCG组和补骨脂组分别与模型组比较，脱色面积指数差异均有统计学意义（均P < 0.05）；同时，EGCG组和补骨脂组非用药部位的脱色面积指数差异同样有统计学意义（P < 0.05）。EGCG组和补骨脂组CD8+ T细胞表达量均低于模型组，EGCG组和补骨脂组差异亦有统计学意义（P < 0.05）。 结论 EGCG和补骨脂对莫诺苯宗诱导的小鼠皮肤和毛发脱色均有干预作用，EGCG的干预作用比补骨脂的干预作用强，该动物模型与人类白癜风具有极高相似性。

关键词: 白癜风, 没食子酸丙酯, 补骨脂, 疾病模型，动物

Abstract: Wang Cui *, Zhu Yiping, Xu Ai′e. *Hangzhou Clinical College Affiliated to Anhui Medical University, Hangzhou 310009, China Corresponding author: Xu Ai′e, Email: xuaiehz@msn.com 【Abstract】 Objective To study the effect of epigallocatechin gallate （EGCG） and fructus psoraleae on the induction of vitiligo-like depigmentation by monobenzone in mice. Methods Forty C57BL/6 mice were included in this study. Hairs in an area measuring 2 cm × 2 cm in size were shaved on the back of each of these mice. Then, the mice were randomly and equally divided into four groups to be topically treated with vaseline cream （negative control group）, monobenzone 40% cream （model group）, EGCG 5% cream followed by monobenzone 40% cream （EGCG group）, fructus psoraleae 7% cream followed by monobenzone 40% cream （fructus psoraleae group）, on the shaved area, respectively, for 50 consecutive days. Depigmentation of skin and hairs was observed daily by naked eyes for 15 days after drug withdrawal. At the end of the study, all the mice were sacrificed, and skin specimens were resected from the tested regions in them. Hematoxylin and eosin （HE） staining was performed to observe lymphocyte infiltration, and immunofluorescence assay to estimate the frequency of CD8+ T cells. Results Depigmentation was observed in monobenzone-induced and -uninduced sites in the model group, and in monobenzone-induced sites in all the mice in the EGCG group and fructus psoraleae group, but in neither monobenzone-induced nor -uninduced sites ih the negative control group. The average time for the appearance of depigmentation at monobenzone-induced sites was 16.7, 29.3 and 19.9 days in the model group, EGCG group and fructus psoraleae group respectively. The depigmentation area index at monobenzone-induced sites was 4.00 ± 0.00 in the model group, significantly different from that in the EGCG group and fructus psoraleae group （2.11 ± 0.54 and 2.84 ± 0.79, both P < 0.05）. Significant differences were also observed in depigmentation area index at monobenzone-induced sites among the model group, EGCG group and fructus psoraleae group （F = 14.173, P < 0.05）, and at monobenzone-uninduced sites between fructus psoraleae group and EGCG group （P < 0.05）. The frequency （expressed as fluorescence intensity） of CD8+ T cells was significantly lower in the EGCG group and fructus psoraleae group than in the model group, and significantly different between EGCG group and fructus psoraleae group （P < 0.05）. Conclusions Both EGCG and fructus psoraleae, especially EGCG, can interfere with the induction of vitiligo-like depigmentation of skin and hairs by monobenzone in mice. The mouse model of vitiligo-like depigmentaion in this study shows higher similarity to human vitiligo.

Key words: Vitiligo, Propyl gallate, PSORALEA CORYLIFOLIA, Disease models, animal