MAPK/ERK and NF-κB Signaling Pathways Mediate Attenuation of Psoriasis by Punicalagin

Abstract

Psoriasis is a chronic autoimmune skin disorder characterized by the rapid and excessive growth of skin cells. It is a non-contagious condition that results in the formation of thick, red, and scaly patches on the skin surface. Psoriasis can affect various parts of the body and is often associated with other health issues. Wang and colleagues explored the impact and molecular mechanism of punicalagin (PU) on M5-stimulated keratinocyte cell lines and imiquimod (IMQ)-induced psoriasis-like skin inflammation in BABL/c mice. Their findings reveal that several indicators of psoriasis and its severity such as splenomegaly, IMQ-induced abnormal epidermal proliferation, CD4+ T-cell infiltration, and inflammatory factor expression were abrogated by  PU-enriched pomegranate extract at dosages of 150 and 250 mg/kg/day. The expression levels of pro-inflammatory cytokines, such as IL-1β, IL-1α, IL-6, IL-8, TNF-α, IL-17A, IL-22, IL-23A, and reactive oxygen species (ROS) were also decreased. This was followed by the inhibition of keratinocyte proliferation in the M5-stimulated cell line model of inflammation. This keratinocyte proliferation inhibition is believed to be mediated through the inhibition of mitogen-activated protein kinases/extracellular regulated protein kinases (MAPK/ERK) and nuclear factor kappa B (NF-κB) signaling pathways. Their findings suggest that PU may serve as a promising nutritional intervention for psoriasis by ameliorating cellular oxidative stress and inflammation. Phytother Res. 2023 Nov 27. doi: 10.1002/ptr.8071.