Coptisine Alleviates Imiquimod-Induced Psoriasis-like Skin Lesions and Anxiety-like Behavior in Mice

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-alpha, 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-alpha and IL-1 beta 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-3 alpha/CCL20, IP-10/CXCL10, and ICAM-1 and suppressed the NF-kappa B signaling pathway. In LPS-stimulated BV2 cells, coptisine reduced the secretion of TNF-alpha and IL-1 beta. These findings suggest that coptisine might be a potential candidate for psoriasis treatment by improving both disease severity and psychological comorbidities.

Automated summary

Coptisine is found to be effective in alleviating psoriasis-like skin lesions, reducing inflammatory cytokine levels, and improving anxiety symptoms. Additionally, in vitro studies show that coptisine can inhibit the production and secretion of inflammatory cytokines in skin cells and microglial cells.