Silymarin exerts antipsoriatic effects against imiquimod-induced psoriasis in mice via NF-kB/TLR4 signaling pathway.

OBJECTIVES

Psoriasis is an autoimmune disease that mainly affects the skin and joints, which is mediated via T-cells. Several factors contribute to its pathogenesis, including genetic and environmental triggers, as well as intrinsic immune processes that lead to an autoimmune response. Silymarin, a flavonoid complex extracted from Silybum marianum, exhibits anti-inflammatory, immunostimulatory, and anti-oxidant properties, rendering it a viable candidate for treating psoriasis. This study aimed to investigate the effect of silymarin on imiquimod (IMQ) induced psoriasis-like skin lesions in male mice applied as a cream for seven consecutive days (1 mg per mouse).

MATERIALS AND

METHODS

Thirty-five male mice were assigned to seven groups (n=5 per group): (I) control group, (II) IMQ group, (III-V) oral silymarin groups (30, 60, and 120 mg/kg), (VI) topical betamethasone group, and (VII) topical silymarin 2% group.

RESULTS

Silymarin, both orally and topically, significantly reduces erythema, thickness, and scaling induced by IMQ after seven days of treatment. The treatment also reversed the increase in spleen weight/body weight ratio. Immunofluorescence analysis revealed that silymarin reduced the expression of nuclear factor κB (NF-κB) (P<0.01) and toll-like receptor 4 (TLR4) (P<0.01) compared to the IMQ group.

CONCLUSION

These findings suggest that silymarin effectively alleviates psoriasis lesions by reducing inflammation and modulating the TLR4/ NF-κB signaling pathway.