Abstract：
BACKGROUND: Current animal models of sensitive skin do not adequately reflect the objective symptoms or physiological manifestations observed in human sensitive skin.
OBJECTIVE: To construct and validate a sensitive skin model in mice.
METHODS: 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.
RESULTS: 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.
CONCLUSIONS: 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.
OBJECTIVE: To construct and validate a sensitive skin model in mice.
METHODS: 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.
RESULTS: 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.
CONCLUSIONS: 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.
摘要：
背景:目前的敏感性皮肤动物模型不能充分反映在人类敏感性皮肤中观察到的客观症状或生理表现。
目的：构建并验证小鼠敏感皮肤模型。
方法:胶带剥离(TS)用于诱导脂质膜和角质层的部分机械破坏。随后，丙二醇（PG）用于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素1（TRPV1）受体，以模拟敏感皮肤的形成。明显的瘙痒和刺痛感，鳞状皮肤,血管舒张,局部拥堵，增加的经皮水分流失（TEWL），TRPV1表达升高，随后评估炎症症状。
结果：TS结合PG和CS应用导致皮肤剥落；皮肤屏障破坏；血管扩张；瘙痒增加，刺痛,和炎症；表皮中TRPV1上调；以及乳酸诱导的瘙痒和刺痛的显着增加。
结论：使用TS和PG的组合，和CS应用程序，成功建立了包括各种皮肤表型和生理表现的敏感皮肤小鼠模型，包括皮肤片，血管舒张,血流量和TEWL增加，瘙痒和刺痛的感觉，炎症,和升高的TRPV1表达。
目的：构建并验证小鼠敏感皮肤模型。
方法:胶带剥离(TS)用于诱导脂质膜和角质层的部分机械破坏。随后，丙二醇（PG）用于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素1（TRPV1）受体，以模拟敏感皮肤的形成。明显的瘙痒和刺痛感，鳞状皮肤,血管舒张,局部拥堵，增加的经皮水分流失（TEWL），TRPV1表达升高，随后评估炎症症状。
结果：TS结合PG和CS应用导致皮肤剥落；皮肤屏障破坏；血管扩张；瘙痒增加，刺痛,和炎症；表皮中TRPV1上调；以及乳酸诱导的瘙痒和刺痛的显着增加。
结论：使用TS和PG的组合，和CS应用程序，成功建立了包括各种皮肤表型和生理表现的敏感皮肤小鼠模型，包括皮肤片，血管舒张,血流量和TEWL增加，瘙痒和刺痛的感觉，炎症,和升高的TRPV1表达。
