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Correlation between the capsaicin test and objective skin measurements in evaluating sensitive skin in Chinese females

机译:辣椒素测试与客观皮肤测量在评估中国女性敏感皮肤中的相关性

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Tacrolimus, a topical calcineurin inhibitor, is an immunosup-pressive drug mainly through down-regulation of T cell activation. Topical application of tacrolimus shows therapeutic effect on inflammatory skin diseases such as atopic dermatitis [1 ]. However, there has been a concern about the long term risk of possible skin cancers facilitated by topical tacrolimus, because of its potential suppression of anti-tumor immunity [2]. Recent studies demonstrated that topical pimecrolimus and tacrolimus did not accelerate photocarcinogenesis in hairless mice after UVA or simulated solar radiation [3,4]. In this study, we examined whether or not topical tacrolimus affected the photocarcinogenesis in cancer-prone, K5.Stat3C transgenic mice. Expression of the Stat3C transgene in the keratinocytes allowed them to develop not only psoriasis-like lesion [5], but also squamous cell carcinoma (SCC) through repeated UVB irradiation [6], since Stat3 activation leads to tumor initiation and promotion [7]. Following UVB irradiation, the formation of skin tumors in K5.Stat3C mice is accelerated and both the incidence and multiplicity of skin tumors are significantly greater than wild-type controls [6]. K5.Stat3C mice develop UVB-induced SCC in situ as early as 14 weeks of UVB irradiation, while more than 25 weeks are required in wild-type mice [6-8]. Therefore, the skin cancer-prone K5.Stat3C mice represent a suitable model for early photocarcinogenesis, thereby any impact of immunosuppressive drug could be easily detected.
机译:他克莫司是一种局部钙调神经磷酸酶抑制剂,主要是通过下调T细胞活化来抑制免疫。他克莫司的局部应用对炎性皮肤疾病如特应性皮炎显示出治疗效果[1]。但是,由于他克莫司可能抑制抗肿瘤免疫力,因此长期关注他克莫司可能引起的皮肤癌的长期风险[2]。最近的研究表明,局部用吡美莫司和他克莫司在UVA或模拟太阳辐射后不会促进无毛小鼠的光致癌作用[3,4]。在这项研究中,我们检查了局部他克莫司是否影响易癌的K5.Stat3C转基因小鼠的光致癌作用。 Stat3C转基因在角质形成细胞中的表达不仅使它们发展为牛皮癣样病变[5],而且通过反复的UVB照射也使它们发展成鳞状细胞癌(SCC)[6],因为Stat3激活导致了肿瘤的发生和促进[7]。 。 UVB照射后,K5.Stat3C小鼠皮肤肿瘤的形成被加速,皮肤肿瘤的发生率和多样性明显高于野生型对照[6]。 K5.Stat3C小鼠最早在UVB照射14周后就可原位形成UVB诱导的SCC,而野生型小鼠则需要超过25周的时间[6-8]。因此,易患皮肤癌的K5.Stat3C小鼠代表了早期光致癌作用的合适模型,因此可以轻松检测到免疫抑制药物的任何影响。

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