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牛磺酸与多酚复合物通过调节IL8和TIMP2表达修复表皮角质形成细胞伤口。

Taurine and Polyphenol Complex Repaired Epidermal Keratinocyte Wounds by Regulating IL8 and TIMP2 Expression.

作者信息

Lee Sooyeon, Shin Jae Young, Kwon Oh Sun, Jun Seung-Hyun, Kang Nae-Gyu

机构信息

LG Household & Health Care (LG H&H) R&D Center, 70, Magokjoongang 10-ro, Gangseo-gu, Seoul 07795, Republic of Korea.

出版信息

Curr Issues Mol Biol. 2024 Aug 8;46(8):8685-8698. doi: 10.3390/cimb46080512.

Abstract

The healing process after acne lesion extraction provides a miniature model to study skin wound repair mechanisms. In this study, we aimed to identify solutions for acne scars that frequently occur on our faces. We performed acne scar cytokine profiling and found that Interleukin 8 (IL8) and Tissue inhibitor of metalloproteinases 2 (TIMP2) were significant factors at the wounded site. The effect of chlorogenic acid and taurine on human epidermal cells and irritated human skin was investigated. Chlorogenic acid and taurine regulated IL8 and TIMP2 expression and accelerated keratinocyte proliferation. Moreover, tight junction protein expression was upregulated by chlorogenic acid and taurine synergistically. Further, these compounds modulated the expression of several inflammatory cytokines (IL1α, IL1β, and IL6) and skin hydration related factor (hyaluronan synthase 3; HAS3). Thus, chlorogenic acid and taurine may exert their effects during the late stages of wound healing rather than the initial phase. In vivo experiments using SLS-induced wounds demonstrated the efficacy of chlorogenic acid and taurine treatment compared to natural healing, reduced erythema, and restored barrier function. Skin ultrasound analysis revealed their potential to promote denser skin recovery. Therefore, the wound-restoring effect of chlorogenic acid and taurine was exerted by suppression of inflammatory cytokines, and induction of cell proliferation, tight junction expression, and remodeling factors.

摘要

痤疮皮损清除后的愈合过程为研究皮肤伤口修复机制提供了一个微型模型。在本研究中,我们旨在找到解决频繁出现在我们面部的痤疮疤痕的方法。我们进行了痤疮疤痕细胞因子分析,发现白细胞介素8(IL8)和金属蛋白酶组织抑制剂2(TIMP2)是伤口部位的重要因素。研究了绿原酸和牛磺酸对人表皮细胞和受刺激的人皮肤的影响。绿原酸和牛磺酸调节IL8和TIMP2的表达,并加速角质形成细胞的增殖。此外,绿原酸和牛磺酸协同上调紧密连接蛋白的表达。此外,这些化合物调节了几种炎症细胞因子(IL1α、IL1β和IL6)和皮肤水合相关因子(透明质酸合酶3;HAS3)的表达。因此,绿原酸和牛磺酸可能在伤口愈合的后期而非初始阶段发挥作用。使用SLS诱导伤口的体内实验证明,与自然愈合相比,绿原酸和牛磺酸治疗具有疗效,可减少红斑并恢复屏障功能。皮肤超声分析显示它们具有促进皮肤更致密恢复的潜力。因此,绿原酸和牛磺酸的伤口修复作用是通过抑制炎症细胞因子以及诱导细胞增殖、紧密连接表达和重塑因子来实现的。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9ba9/11352352/d51a922baac1/cimb-46-00512-g001.jpg

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