背景:银屑病的发病机制涉及角质形成细胞和免疫细胞之间的相互作用,导致免疫失衡。虽然目前大多数临床治疗方案都能快速缓解症状,它们经常伴随着显著的副作用。四角大红多糖(THP),天然无毒,具有显著的免疫调节和抗炎特性。
方法:在本研究中,我们使用了咪喹莫特(IMQ)诱导的银屑病小鼠模型和LPS/IL-6刺激的HaCaT模型。通过包括银屑病面积严重程度指数(PASI)评分在内的方法评估THP在银屑病治疗中的潜力和作用机制。组织病理学,流式细胞术,免疫印迹,和逆转录-聚合酶链反应(RT-PCR)。
结果:经皮给药THP可显着缓解IMQ诱发的银屑病小鼠的症状和表现,包括银屑病皮肤外观的改善(红斑,折叠,scales),组织病理学变化,PASI分数下降,和脾脏指数。此外,THP抑制Th17细胞的异常增殖和角质形成细胞的过度增殖和炎症。此外,THP表现出调节JAK/STAT3信号通路的能力。
结论:体内和体外研究的结果表明,THP可以抑制病变皮肤的异常细胞增殖和过度炎症,平衡Th17免疫细胞,并破坏角质形成细胞和Th17细胞之间的相互作用。这种作用机制可能涉及JAK/STAT3信号通路的调节,提供牛皮癣治疗的潜在影响。
BACKGROUND: The pathogenesis of psoriasis involves the interaction between keratinocytes and immune cells, leading to immune imbalance. While most current clinical treatment regimens offer rapid symptom relief, they often come with significant side effects. Tetrastigma hemsleyanum polysaccharides (THP), which are naturally nontoxic, possess remarkable immunomodulatory and anti-inflammatory properties.
METHODS: In this study, we utilized an
imiquimod (IMQ)-induced psoriasis mouse model and a LPS/IL-6-stimulated HaCaT model. The potential and mechanism of action of THP in psoriasis treatment were assessed through methods including Psoriasis Area Severity Index (PASI) scoring, histopathology, flow cytometry, immunoblotting, and reverse transcription-polymerase chain reaction (RT-PCR).
RESULTS: Percutaneous administration of THP significantly alleviated symptoms and manifestations in IMQ-induced psoriatic mice, including improvements in psoriatic skin appearance (erythema, folds, scales), histopathological changes, decreased PASI scores, and spleen index. Additionally, THP suppressed abnormal proliferation of Th17 cells and excessive proliferation and inflammation of keratinocytes. Furthermore, THP exhibited the ability to regulate the JAK/STAT3 signaling pathway.
CONCLUSIONS: Findings from in vivo and in vitro studies suggest that THP can inhibit abnormal cell proliferation and excessive inflammation in lesional skin, balance Th17 immune cells, and disrupt the interaction between keratinocytes and Th17 cells. This mechanism of action may involve the modulation of the JAK/STAT3 signaling pathway, offering potential implications for psoriasis treatment.