Attenuated effects of topical vinpocetine in an imiquimod-induced mouse model of psoriasis

Mitigative Effects of Topical Norfloxacin on an Imiquimod-Induced Murine Model of Psoriasis

“…The prototype of imiquimod-aggravated psoriasis in mice is more broadly utilized for experiments on molecular processes, antipsoriatic medication development, and percutaneous drug absorption. ,,, In tandem with past investigations, an 8-day administration of imiquimod to mouse dorsal skinfolds gave rise to psoriasiform plaques characterized by redness, desquamation, and acanthosis, along with upregulated expression of pro-inflammatory, angiogenic, and oxidative parameters. ,,, …”

“…Previous studies have indicated that erythema signifies the degree of cutaneous vasodilation that is compounded by dendritic cells, mast cells, and keratin cells, all of which are believed to generate elements that cause inflammation, involving histamine and nitric oxide. , Pro-inflammatory cytokines trigger keratinocyte proliferation, leading to skin induration. White-gray peelings built up as a consequence of keratinocyte improper differentiation. ,, …”

“…Psoriasis is heavily influenced by cytokines produced by Th1 cells (IFN-γ, IL-1β, IL-6, and TNF-α) and dendritic cells (IL-10, IL-17, IL-22, and IL-23). All of these cytokines have the potential to be psoriatic indicators. , However, the two primary strategies for addressing psoriasis can be identified as topical drugs (corticosteroids and vitamin D3 derivatives) and systemic drugs (retinoids like acitretin, PDE inhibitors like apremilast, antimetabolites like methotrexate, immunosuppressive drugs like cyclosporine, phototherapies like PUVA, and biologics like etanercept, infliximab, bimekizumab, and guselkumab). − …”