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

Abstract

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 in vitro, 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.