Cinnamaldehyde inhibits psoriasis‑like inflammation by suppressing proliferation and inflammatory response of keratinocytes via inhibition of NF‑κB and JNK signaling pathways

• Published in: Molecular medicine reports Vol. 24; no. 3
• Main Authors: Ding, Zhenzhen, Liu, Jingjing, Qian, Huangjing, Wu, Lingjian, Lv, Mingfen
• Format: Journal Article
• Language: English
• Published: Greece Spandidos Publications UK Ltd 01.09.2021; D.A. Spandidos
• Subjects: Acrolein - analogs & derivatives; Acrolein - antagonists & inhibitors; Acrolein - pharmacology; Biotechnology; Cell cycle; Cell differentiation; Cell Differentiation - drug effects; Cell Line; Cell proliferation; Cell Proliferation - drug effects; Cinnamaldehyde; Cytokines; Cytokines - metabolism; Down-Regulation; Epidermis - metabolism; Filaggrin; Flow cytometry; Humans; Inflammation; Inflammation - drug therapy; Inflammatory diseases; Interleukin 22; Keratin; Keratinocytes; Keratinocytes - metabolism; Laboratories; MAP Kinase Signaling System; NF-kappa B - metabolism; NF-κB protein; Oncostatin M; Oxidative Stress; Phosphorylation; Proteins; Psoriasis; Psoriasis - drug therapy; Signal transduction; Signal Transduction - drug effects; Software; Tumor Necrosis Factor-alpha - metabolism; Tumor necrosis factor-α; Western blotting; cinnamaldehyde; hyperproliferation; keratinocytes; inflammation; psoriasis
• ISSN: 1791-2997; 1791-3004
• DOI: 10.3892/mmr.2021.12277

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.