哈卡特
银屑病
炎症
白细胞介素17
下调和上调
白细胞介素
免疫印迹
医学
药理学
脂多糖
免疫学
化学
细胞因子
体外
生物化学
基因
作者
Penghui Li,Yonglian Li,Hong Jiang,Yuting Xu,Xiaoying Liu,Biao Che,Jian Tang,Guangrong Liu,Yadong Tang,Wei Zhou,Langyue Zhang,Chang‐Zhi Dong,Huixiong Chen,Kun Zhang,Zhiyun Du
标识
DOI:10.1016/j.intimp.2018.04.018
摘要
In this paper, we investigate the effect of glabridin (Glab) on psoriasis. We observed that Glab significantly suppressed the levels of nitric oxide (NO), NF-κB subunit p65, interleukin (IL)-6, and IL-1β in lipopolysaccharide (LPS)-stimulated HaCaT cells. In addition, Glab treatment reduced the expression of IL-17A, IL-22, and IL-23 in TNF-α-stimulated-HaCaT cells. These findings prompted us to test whether Glab could be used to treat psoriasis in vivo. The effects of Glab on PASI scores, histopathological changes, oxidative/anti-oxidative indexes and pro-inflammatory cytokines in IMQ-induced mice were investigated. The results indicated that Glab could reduce the PASI scores and ameliorate the deteriorating histopathology. Interestingly, RT-PCR revealed that Glab significantly decreased the mRNA expression of p65, IL-6, IL-1β, IL-17A, IL-22, and IL-23. These results were confirmed by Western blot analysis and immunohistochemistry staining. In conclusion, our present study revealed that Glab had beneficial effects on psoriasis, and the underlying mechanism may be associated with the downregulation of pro-inflammatory cytokines and the improvement of antioxidant status. Hence, Glab is a promising candidate molecule for development of effective psoriasis therapies.
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