Huang Bingli, Wang Xueer, Bu Lingwei, Zhang Yarui, Liu Xiaoran, Liang Fengting, Zhang Xinyue, Tang Xueting, Wu Shenhua, Huang Jianyuan, Zhang Lin, Zhang Min
School of Public Health, Southern Medical University, Guangzhou, China.
GDMPA Key Laboratory of Key Technologies for Cosmetics Safety and Efficacy Evaluation, NMPA Key Laboratory for Safety Evaluation of Cosmetics, Guangdong Provincial Key Laboratory of Construction and Detection in Tissue Engineering, Department of Histology and Embryology, School of Basic Medical Sciences, Southern Medical University, Guangzhou, China.
Contact Dermatitis. 2024 Oct;91(4):327-341. doi: 10.1111/cod.14652. Epub 2024 Jul 30.
Current animal models of sensitive skin do not adequately reflect the objective symptoms or physiological manifestations observed in human sensitive skin.
To construct and validate a sensitive skin model in mice.
Tape stripping (TS) was used to induce partial mechanical disruption of the lipid film and stratum corneum. Subsequently, propylene glycol (PG) was applied to disrupt the lipid structure in the skin barrier, and capsaicin (CS) activate transient receptor potential vanilloid 1 (TRPV1) receptors of keratinocytes to simulate the formation of sensitive skin. Evident itching and tingling sensations, scaly skin, vasodilation, local congestion, increased transepidermal water loss (TEWL), elevated TRPV1 expression, and inflammatory symptoms were subsequently evaluated.
TS combined with PG and CS application resulted in skin flakes; skin barrier disruption; vascular dilation; increased itching, stinging, and inflammation; TRPV1 upregulation in the epidermis; and a significant increase in lactic acid-induced itching and stinging.
Using a combination of TS and PG, and CS application, a mouse model of sensitive skin was successfully established involving various skin phenotypes and physiological manifestations, including skin flakes, vasodilation, increased blood flow and TEWL, itching and stinging sensations, inflammation, and elevated TRPV1 expression.
目前的敏感性皮肤动物模型不能充分反映人类敏感性皮肤所观察到的客观症状或生理表现。
构建并验证小鼠敏感性皮肤模型。
采用胶带剥离法(TS)诱导脂质膜和角质层的部分机械性破坏。随后,应用丙二醇(PG)破坏皮肤屏障中的脂质结构,辣椒素(CS)激活角质形成细胞的瞬时受体电位香草酸亚型1(TRPV1)受体以模拟敏感性皮肤的形成。随后评估明显的瘙痒和刺痛感、皮肤脱屑、血管舒张、局部充血、经表皮水分流失(TEWL)增加、TRPV1表达升高以及炎症症状。
TS联合应用PG和CS导致皮肤脱屑、皮肤屏障破坏、血管扩张、瘙痒、刺痛和炎症增加、表皮TRPV1上调以及乳酸诱导的瘙痒和刺痛显著增加。
通过联合应用TS、PG和CS,成功建立了一种涉及多种皮肤表型和生理表现的小鼠敏感性皮肤模型,包括皮肤脱屑、血管扩张、血流和TEWL增加、瘙痒和刺痛感、炎症以及TRPV1表达升高。