Psoriasis is a common inflammatory skin disorder, which can be associated with psychological disorders, such as anxiety and depression. This study investigated the efficacy and the mechanism of action of a natural compound
coptisine using
imiquimod (IMQ)-induced
psoriasis mice.
Coptisine reduced the severity of
psoriasis-like skin lesions, decreased epidermal
hyperplasia and the levels of inflammatory
cytokines TNF-α,
IL-17, and
IL-22. Furthermore,
coptisine improved IMQ-induced anxiety in mice by increasing the number of entries and time in open arms in the elevated plus maze (EPM) test.
Coptisine also lowered the levels of inflammatory
cytokines TNF-α and IL-1β in the prefrontal cortex of
psoriasis mice. HaCaT keratinocytes and BV2 microglial cells were used to investigate the effects of
coptisine in vitro. In M5-treated HaCaT cells,
coptisine decreased the production of
IL-6, MIP-3α/CCL20, IP-10/CXCL10, and
ICAM-1 and suppressed the NF-κB signaling pathway. In LPS-stimulated BV2 cells,
coptisine reduced the secretion of TNF-α and IL-1β. These findings suggest that
coptisine might be a potential candidate for
psoriasis treatment by improving both disease severity and psychological comorbidities.