Tetrastigma hemsleyanum Polysaccharides Alleviate Imiquimod-Induced Psoriasis-Like Skin Lesions in Mice by Modulating the JAK/STAT3 Signaling Pathway

Crosstalk between keratin-forming cells and aberrant immune cells due to immune imbalance is a key factor in the pathogenesis of psoriasis. Most of the current clinical treatments provide rapid symptomatic relief but bring side effects that should not be ignored. Tetrastigma hemsleyanum polysaccharides (THP) have significant immunomodulatory and anti-inflammatory properties. In this study, we used imiquimod (IMQ)-induced psoriasis mouse model and LPS/IL-6-stimulated HaCaT cell model. The potential and mechanism of action of THP for psoriasis treatment were assessed by Psoriasis Area Severity Index (PASI) score, histopathology, flow cytometry, Western blot, and reverse transcription-polymerase chain reaction. The signs and symptoms of psoriatic mice induced by IMQ were significantly relieved by percutaneous administration of THP, including the improvement of psoriatic skin signs (erythema, folds, scales), pathological changes, decreased PASI score, and decreased spleen index. Results of in vivo and in vitro studies suggest that THP inhibits abnormal cell proliferation and excessive inflammation at skin lesions, balances Th17 immune cells, and blocks the keratinocyte-Th17 cell cycle, thus playing a role in psoriasis treatment by a mechanism that may be related to the regulation of the JAK/STAT3 signaling pathway.