特应性皮炎(AD),慢性炎症性疾病,严重干扰病人的生活。人胎盘提取物(HPH;也称为人胎盘水解物)是各种生物活性物质的丰富来源,已被广泛用于抑制炎症,改善疲劳,发挥抗衰老作用,促进伤口愈合。然而,关于HPH纳入AD治疗的信息有限。因此,这项研究旨在评估HPH在使用肿瘤坏死因子(TNF)-α/干扰素(IFN)-γ刺激的人角质形成细胞(HaCaT)治疗AD中的有效潜力,免疫脾细胞,和2,4-二硝基氯苯(DNCB)诱导的AD小鼠模型。在TNF-α/IFN-γ刺激的HaCaT细胞中,HPH显着减少活性氧(ROS)的产生并恢复核因子红系2相关因子2(Nrf2)的表达,超氧化物歧化酶1(SOD1),过氧化氢酶,和聚丝(FLG)。HPH减少白细胞介素(IL)-6;胸腺和激活调节趋化因子(TARC);胸腺基质淋巴细胞生成素(TSLP);并在激活时调节,正常T细胞表达和推测分泌(RANTES)水平并抑制核因子κB磷酸化。此外,HPH抑制免疫脾细胞中的T辅助细胞2(Th2)免疫应答。在类似AD的小鼠模型中,它显著减轻了DNCB诱导的浸润肥大细胞和巨噬细胞的升高,表皮厚度,和AD症状。HPH还降低TSLP水平并阻止FLG下调。此外,它降低了IL-4,IL-5,IL-13,TARC的表达水平,RANTES,血清和AD样皮肤病变中的免疫球蛋白E(IgE)。总的来说,我们的研究结果表明,HPH能有效抑制AD的发展,是治疗AD样皮肤病的潜在药物.
Atopic dermatitis (AD), a chronic inflammatory disease, severely interferes with patient life. Human placenta extract (HPH; also known as human placenta hydrolysate) is a rich source of various bioactive substances and has widely been used to dampen inflammation, improve fatigue, exert anti-aging effects, and promote wound healing. However, information regarding HPH\'s incorporation in AD therapies is limited. Therefore, this study aimed to evaluate HPH\'s effective potential in treating AD using tumor necrosis factor (TNF)-α/interferon (IFN)-γ-stimulated human keratinocytes (HaCaT), immunized splenocytes, and a 2,4-dinitrochlorobenzene (DNCB)-induced AD mouse model. In TNF-α /IFN-γ-stimulated HaCaT cells, HPH markedly reduced the production of reactive oxygen species (ROS) and restored the expression of nuclear factor erythroid 2-related factor 2 (Nrf2), superoxide dismutase 1(SOD1), catalase, and filaggrin (FLG). HPH reduced interleukin (IL)-6; thymus- and activation-regulated chemokine (TARC); thymic stromal lymphopoietin (TSLP); and regulated upon activation, normal T cell expressed and presumably secreted (RANTES) levels and inhibited nuclear factor kappa B phosphorylation. Additionally, HPH suppressed the T helper 2 (Th2) immune response in immunized splenocytes. In the AD-like mouse model, it significantly mitigated the DNCB-induced elevation in infiltrating mast cells and macrophages, epidermal thickness, and AD symptoms. HPH also reduced TSLP levels and prevented FLG downregulation. Furthermore, it decreased the expression levels of IL-4, IL-5, IL-13, TARC, RANTES, and immunoglobulin E (IgE) in serum and AD-like skin lesion. Overall, our findings demonstrate that HPH effectively inhibits AD development and is a potentially useful therapeutic agent for AD-like skin disease.