Taxifolin attenuates IMQ-induced murine psoriasis-like dermatitis by regulating T helper cell responses via Notch1 and JAK2/STAT3 signal pathways

Abstract

Psoriasis is a T cells mediated chronic skin inflammation in which helper T (Th) cells play in critical roles in its pathogenesis. Taxifolin (TXL) has been discovered to exert various pharmacological activities. In this study, we wished to observe whether TXL had potential activities on psoriasis, and how it works. We found that TXL can inhibit LPS-induced abnormal proliferation in Hacat cell line, ant also significantly alleviate the IMQ-induced psoriasis in BALB/c mice, comparing with the control group. Although TXL has no significant effects on the ratio of total T cells in skin draining lymph nodes (SDLN), it decreases the ratio of pro-inflammatory Th1 and Th17 cells, both in skin lesions and SDLN. Our results also disclosed that TXL may regulate Th cells differentiation by inhibiting the transcript factors, including T-bet, GATA-3 and RORγt. Further data show that TXL can inhibit Notch1 and Jak2/Stat3 signal pathways. In summary, TXL may be able to treat psoriasis by regulating Th cells differentiation via inhibiting Notch1 and Jak2/Stat3 pathways.

Keywords: JAK2/STAT3 signal pathway; Notch1 signal pathway; Psoriasis; T helper cell responses; Taxifolin.