背景:牛皮癣是指一种高度流行和免疫介导的皮肤病,其生活质量明显下降。Wogonin,一种类黄酮,已被提及在皮肤疾病中引发保护活性。然而,Wogonin是否参与银屑病的治疗及其具体机制尚不完全清楚。
目的:本文试图阐述汉黄芩素在银屑病发病过程中的作用及相关作用机制。
方法:最初应用细胞计数试剂盒-8(CCK-8)方法来测定通过不同浓度的Wogonin处理的人角质形成细胞HaCaT细胞的活力。体外模拟银屑病,将HaCaT细胞暴露于M5细胞因子。CCK-8和5-乙炔基-2'-脱氧尿苷测定法用于测量细胞增殖。用酶联免疫吸附测定检查炎症水平。免疫荧光染色测试了核苷酸结合寡聚化结构域(NOD)样受体家族pyrin结构域包含3(NLRP3)和Caspase-1的表达。Westernblot检查了增殖的蛋白质表达-,炎症-,焦亡相关因素,NLRP3。
结果:Wogonin治疗可拮抗增殖,炎症反应,和NLRP3/caspase-1/Gasdermin-D(GSDMD)介导的M5攻击的HaCaT细胞中的焦亡。此外,NLRP3升高部分消除了Wogonin对M5诱导的增殖的影响,炎症反应,和NLRP3/caspase-1/GSDMD介导的HaCaT细胞中的焦亡。
结论:总之,Wogonin可能发挥抗增殖作用,在M5诱导的银屑病细胞模型中的抗炎和抗焦亡活性以及NLRP3/Caspase-1/GSDMD通路的阻断可能被认为是Wogonin在银屑病中保护机制的潜在机制。提示Wogonin是一种潜在的抗牛皮癣药物。
BACKGROUND: Psoriasis refers to a highly prevalent and immunologically mediated dermatosis with considerable deterioration in life quality. Wogonin, a sort of flavonoid, has been mentioned to elicit protective activities in skin diseases. However, whether Wogonin is implicated in the treatment of psoriasis and its specific mechanisms are not fully understood.
OBJECTIVE: The present work attempted to elaborate the role of Wogonin during the process of psoriasis and to concentrate on the associated action mechanism.
METHODS: Cell counting kit-8 (CCK-8) method was initially applied to assay the viability of human keratinocyte HaCaT cells treated by varying concentrations of Wogonin. To mimic psoriasis in vitro, HaCaT cells were exposed to M5 cytokines. CCK-8 and 5-Ethynyl-2\'-deoxyuridine assays were adopted for the measurement of cell proliferation. Inflammatory levels were examined with enzyme-linked immunosorbent assay. Immunofluorescence staining tested nucleotide-binding oligomerization domain (NOD)-like receptor family pyrin domain containing 3 (NLRP3) and Caspase-1 expressions. Western blot examined the protein expressions of proliferation-, inflammation-, pyroptosis-associated factors, and NLRP3.
RESULTS: Wogonin treatment antagonized the proliferation, inflammatory response, and NLRP3/caspase-1/Gasdermin-D (GSDMD)-mediated pyroptosis in M5-challenged HaCaT cells. Besides, NLRP3 elevation partially abrogated the effects of Wogonin on M5-induced proliferation, inflammatory response, and NLRP3/caspase-1/GSDMD-mediated pyroptosis in HaCaT cells.
CONCLUSIONS: In a word, Wogonin might exert anti-proliferation, anti-inflammatory and anti-pyroptosis activities in M5-induced cell model of psoriasis and the blockade of NLRP3/Caspase-1/GSDMD pathway might be recognized as a potential mechanism underlying the protective mechanism of Wogonin in psoriasis, suggesting Wogonin as a prospective anti-psoriasis drug.