Amentoflavone protects against psoriasis-like skin lesion through suppression of NF-κB-mediated inflammation and keratinocyte proliferation.

An, Jingang; Li, Zhengxiao; Dong, Yingying; Ren, Jianwen; Huo, Jia

Psoriasis is a one of the most common chronic skin diseases, which affects 0.6-4.8 % of the general population. Amentoflavone (AMF) belongs to the biflavonoid class of flavonoids, possessing various biological effects, such as anti-inflammatory, antioxidant, and anti-apoptotic effects. In the present study, we aimed to investigate the effect of AMF on psoriasis in imiquimod (IMQ) psoriasis-like lesions in mice and keratinocyte proliferation in HaCaT cells. We showed that AMF reduced skinfold thickening, and improved erythema and scaling scores and histological lesions in IMQ-treated mice. AMF exerted potent anti-inflammatory effect via influencing a variety of proinflammatory cytokines, including tumor necrosis factor α, interleukin (IL)-17A, IL-22, and IL-23 in local skin lesions and the whole body. In M5 (a cocktail of cytokines)-treated HaCaT cells, AMF significantly inhibited cell proliferation, promoted apoptosis, and inhibited the increase of expression of cyclin D1, cyclin E, IL-17A, and IL-22. In addition, AMF inhibited the upregulation of p65 NF-κB under psoriatic condition. Moreover, overexpression of p65 NF-κB significantly suppressed the effect of AMF on keratinocyte proliferation, apoptosis, and expression of cyclin D1, cyclin E, IL-17A, and IL-22. These results demonstrated that suppression of NF-κB was involved in AMF-resulted anti-proliferative, apoptosis-promoting, anti-inflammatory effects in keratinocytes. The data demonstrate that AMF may serve as potential therapeutic option for patients with psoriasis.

PSORIASIS; IRRITATION (Pathology); INFLAMMATION; KERATINOCYTE differentiation; COUNTERIRRITATION

Molecular & Cellular Biochemistry, 2016, Vol 413, Issue 1/2, p87

0300-8177

Academic Journal

10.1007/s11010-015-2641-6