LAUSR

Pathological studies have shown an association between psoriasis and renal injury (RI), but the mechanism between RI and psoriasis was still unclear. This paper was designed to investigate the relationship and mechanism between psoriasis-like inflammation and renal injury in BALB/C mice. Mice were topically smeared imiquimod followed by various analyses in skin lesions, urine protein, kidney/serum inflammatory cytokines, kidney function, podocyte membrane proteins, and toll-like receptors/nuclear factor kappa-b (TLR/NF-κB) pathway-associated proteins. Meanwhile, lipopolysaccharide (LPS) and dexamethasone (DEX) were intraperitoneally injected to promote and inhibit inflammation accompanied by imiquimod to elaborate the relevance between inflammatory levels and RI. In the model group, the Psoriasis Area and Severity Index (PASI) scores of scaly and erythema obviously increased (p < 0.01), creatinine and blood urea nitrogen significantly increased (p < 0.01), the positive area of hematoxylin-eosin (HE) and periodic acid-Schiff (PAS) staining in kidney increased (p < 0.01), malondialdehyde significantly increased with superoxide dismutase (SOD) decreased (p < 0.01), 24-hour urine protein increased and the expressions of podocin and CD2 associate protein (CD2AP) decreased (p < 0.01), and kidney/serum inflammatory factors (IL-17, IL-1β, IL-6, TNF-α, and IL-22) and TLR/NF-κB-related expression (TLR2, TLR4, MyD88, and NF-κBp65) all increased (p < 0.01). The RI was aggravated with the TLR/NF-κB related expression being upregulated by LPS (p < 0.05). On the contrary, the RI was alleviated by DEX (p < 0.05). Our data showed that psoriasis-like inflammation damaged the renal function via the TLR/NF-κB signal pathway. Inhibiting TLR/NF-κB-related protein expression may be effective for the treatment of RI caused by psoriasis.