<br>重组丝聚蛋白-2 可改善皮肤屏障功能并减轻紫外线 B （UVB）照射诱导的表皮屏障破坏,International Journal of Biological Macromolecules

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重组丝聚蛋白-2 可改善皮肤屏障功能并减轻紫外线 B （UVB）照射诱导的表皮屏障破坏
International Journal of Biological Macromolecules ( IF 7.7 ) Pub Date : 2024-09-26 , DOI: 10.1016/j.ijbiomac.2024.136064
Zhaoyang Wang ₁ , Hongxia Chen ₁ , Yuxin Wang ₁ , Chunna Wu ₂ , Tao Ye ₂ , Huan Xia ₃ , Rufei Huang ₂ , Jingxian Deng ₂ , Ziyi Li ₂ , Yadong Huang ₄ , Yan Yang ₄

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皮肤屏障的完整性对于维持皮肤健康至关重要，角质层和聚丝蛋白 2 （FLG-2）起着关键作用。FLG-2 缺陷或突变与特应性皮炎等疾病有关，而紫外线 B （UVB）辐射等外部压力源会进一步破坏表皮屏障。本研究探讨了重组聚丝蛋白（rFLG）对皮肤屏障功能和 UVB 诱导的表皮破坏的影响。细胞实验表明，10 μg/mL rFLG 可使 HaCaT 细胞的迁移率从 20 % 提高到 42 %，上皮电阻（TEER）值增加约 2 倍，紧密连接相关蛋白上调约 2 倍。在 UVB 诱导的表皮屏障破坏的小鼠模型中，浓度为 0.5、1 和 2 mg/mL 的 rFLG 显示出有效的细胞摄取和皮肤渗透，减轻了红斑，并将小鼠的皮肤厚度减少了 1.5-3 倍。其中，2 mg/mL rFLG 处理通过使血清羟脯氨酸和超氧化物歧化酶水平正常化，恢复了紧密连接蛋白（LOR、ZO-1 和 caspase-14）的表达，减少了胶原蛋白降解，并降低了氧化应激。此外，2 mg/mL 的 rFLG 抑制 UVB 诱导的基质金属蛋白酶（MMP-3 和 MMP-9）上调，并将促炎因子（IL-10、IL-1α、IL-6 和 TNF-α）和凋亡标志物（P38、Bax 和 Bcl-2）降低至正常水平。这些发现表明，rFLG 有效地增强了皮肤屏障完整性并减轻了 UVB 诱导的表皮屏障破坏，突出了其作为皮肤屏障功能障碍相关疾病治疗剂的潜力。

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Recombinant filaggrin-2 improves skin barrier function and attenuates ultraviolet B (UVB) irradiation-induced epidermal barrier disruption

The integrity of the skin barrier is essential for maintaining skin health, with the stratum corneum and filaggrin 2 (FLG-2) playing a key role. FLG-2 deficiency or mutation has been linked to diseases such as atopic dermatitis, while external stressors such as ultraviolet B (UVB) radiation further damage the epidermal barrier. This study investigated the effects of recombinant filaggrin (rFLG) on skin barrier function and UVB induced epidermal destruction. Cell experiments showed that 10 μg/mL of rFLG could increase the mobility of HaCaT cells from 20 % to 42 %, increase the epithelial resistance (TEER) value by about 2 times, and up-regulate the tight junction associated protein by about 2 times. In mouse models of UVB-induced epidermal barrier destruction, rFLG at concentrations of 0.5, 1, and 2 mg/mL showed effective cell uptake and skin penetration, alleviating erythema, and reducing skin thickness in mice by 1.5–3 times. Among them, 2 mg/mL of rFLG treatment restored the expression of tight junction proteins (LOR, ZO-1, and caspase-14), reduced collagen degradation, and reduced oxidative stress by normalizing serum hydroxyproline and superoxide dismutase levels. In addition, 2 mg/mL of rFLG inhibited UVB-induced upregulation of matrix metalloproteinases (MMP-3 and MMP-9) and reduced pro-inflammatory factors (IL-10, IL-1α, IL-6, and TNF-α) and apoptotic markers (P38, Bax, and Bcl-2) to normal levels. These findings suggested that rFLG effectively enhanced skin barrier integrity and mitigated UVB-induced epidermal barrier destruction, highlighting its potential as a therapeutic agent for diseases associated with skin barrier dysfunction.

更新日期：2024-09-26

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