Eupatilin inhibits keratinocyte proliferation and ameliorates imiquimod-induced psoriasis-like skin lesions in mice via the p38 MAPK/NF-κB signaling pathway.

BACKGROUND

Psoriasis is a chronic inflammatory skin disease that is currently incurable and causes long-term distress to patients. Therefore, there is an urgent need to develop safe and effective psoriatic drugs. Eupatilin is a natural flavone, that has a variety of pharmacological effects. However, the anti-psoriatic effect of eupatilin and its underlying mechanism remain unclear.

METHODS

HaCaT cells were treated with 20 μg/mL LPS for 24 h to establish the proliferation model of HaCaT cells. Cell viability was measured by MTT assay. Western blotting was used to detect the expression of p-p38 MAPK, p38 MAPK, p-NF-κB p65 and NF-κB p65 in HaCaT cells. Imiquimod (IMQ) was used to induce psoriasis-like mouse model. Psoriasis Area Severity Index (PASI) score was used to evaluate the degree of skin injury, H&E staining was used to observe the pathological damage of skin tissues, and the expression levels of TNF-α, IL-6, IL-23 and IL-17 in the serum were detected by enzyme-linked immunosorbent assay (ELISA).

RESULTS

Eupatilin could inhibit the hyperproliferation of LPS-stimulated HaCaT cells through p38 MAPK/NF-κB signaling pathway in vitro. In psoriatic mice, eupatilin could significantly reduce skin erythema, scales and thickening scores, ameliorate skin histopathological lesions, and decrease the levels of TNF-α, IL-6, IL-23 and IL-17 in the serum.

CONCLUSION

Eupatilin had a good anti-proliferative effect in LPS-stimulated HaCaT cells, and significantly alleviated IMQ-induced psoriasis-like lesions in mice. Eupatilin was a promising drug for the treatment of psoriasis.