Department of Dermatovenereology, Yuyao People's Hospital of Zhejiang Province, Yuyao, Zhejiang 315400, P.R. China.
Department of Dermatovenereology, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, Zhejiang 325000, P.R. China.
Mol Med Rep. 2021 Sep;24(3). doi: 10.3892/mmr.2021.12277. Epub 2021 Jul 19.
Psoriasis is a systemic immune‑mediated inflammatory disease characterized by uncontrolled keratinocyte proliferation and poor differentiation. Cinnamaldehyde (CIN) has been shown to inhibit the proliferation and inflammatory response of primary and immortalized immune cells. However, to the best of our knowledge, the role of CIN in the progression of psoriasis remains unclear. Therefore, the present study aimed to investigate the biological role of CIN in psoriasis. To mimic abnormal proliferation and differentiation in keratinocytes , normal human epidermal keratinocytes (NHEKs) were stimulated with M5 (IL‑1α, IL‑17A, IL‑22, oncostatin M and TNF‑α). The viability and proliferation of NHEKs were analyzed using Cell Counting Kit‑8 and 5‑Ethynyl‑2'‑deoxyuridine assays, respectively. Western blotting was used to analyze the expression levels of keratin 1, filaggrin and loricrin in NHEKs. The results of the present study revealed that CIN significantly inhibited the proliferation and cell cycle progression, and promoted the differentiation of M5‑stimulated NHEKs. CIN also markedly attenuated the extent of oxidative stress‑induced damage in M5‑stimulated NHEKs. Moreover, CIN ameliorated M5‑induced inflammatory injury in NHEKs, as evidenced by the decreased levels of multiple inflammatory factors. Furthermore, CIN notably downregulated the expression levels of phosphorylated (p)‑inhibitor of NF‑κB, p‑p65 and p‑JNK in M5‑stimulated NHEKs. In conclusion, the present data suggested that CIN may protect NHEKs against M5‑induced hyperproliferation and inflammatory injury via inhibition of NF‑κB and JNK signaling pathways. These results provide a novel insight on the role of CIN in psoriasis.
银屑病是一种以角质形成细胞不受控制的增殖和分化不良为特征的系统性免疫介导的炎症性疾病。肉桂醛（CIN）已被证明能抑制原代和永生化免疫细胞的增殖和炎症反应。然而，据我们所知，CIN 在银屑病进展中的作用尚不清楚。因此，本研究旨在探讨 CIN 在银屑病中的生物学作用。为了模拟角质形成细胞的异常增殖和分化，用 M5（IL-1α、IL-17A、IL-22、oncostatin M 和 TNF-α）刺激正常人表皮角质形成细胞（NHEKs）。分别用细胞计数试剂盒-8 和 5-乙炔基-2'-脱氧尿苷检测试剂盒分析 NHEKs 的活力和增殖。用 Western blot 分析 NHEKs 中角蛋白 1、兜甲蛋白和桥粒芯糖蛋白的表达水平。本研究结果表明，CIN 显著抑制 M5 刺激的 NHEKs 的增殖和细胞周期进程，并促进其分化。CIN 还显著减轻 M5 刺激的 NHEKs 中氧化应激诱导的损伤程度。此外，CIN 改善了 M5 诱导的 NHEKs 中的炎症损伤，这表现为多种炎症因子水平降低。此外，CIN 显著下调了 M5 刺激的 NHEKs 中磷酸化（p）-NF-κB、p-p65 和 p-JNK 的表达水平。综上所述，本研究数据表明，CIN 可能通过抑制 NF-κB 和 JNK 信号通路来保护 NHEKs 免受 M5 诱导的过度增殖和炎症损伤。这些结果为 CIN 在银屑病中的作用提供了新的见解。
