Potential mechanism of oral baicalin treating psoriasis via suppressing Wnt signaling pathway and inhibiting Th17/IL‐17 axis by activating PPARγ

Abstract

Psoriasis (PSO), an immune‐mediated chronic inflammatory skin disease, has seriously affected the quality of patients' life. It is urgent to find effective medicines with lower costs and less side effects. Baicalin (HQG) is the main bioactive substance from Scutellaria baicalensis with effects of anti‐inflammation and immunoregulation. Herein, we explored the effect of oral HQG treating PSO and its potential mechanism. Firstly, network pharmacology was used to predict that HQG may act on Estrogen, TNF‐alpha (tumor necrosis factor, TNF), interleukin‐17 (IL‐17) signaling pathways and Th17 cell differentiation, especially the key targets including TNF, Proto‐oncogene tyrosine‐protein kinase Src, Peroxisome proliferator‐activated receptor gamma and Matrix metalloproteinase‐9. Imiquimod (IMQ)‐induced mice were then used to study the effects of HQG treating PSO. HQG could significantly ameliorate the skin lesions, decrease the level of inflammatory factors and inhibit Th1/Th17 cell differentiation in IMQ‐induced mice. Finally, transcriptome analysis of skin lesions integrated with the prediction of network pharmacology further demonstrated that the potential mechanism may be associated with suppressing Wnt signaling pathway and inhibiting Th17/IL‐17 axis by activating PPARγ. In conclusion, this study suggested that HQG may be a promising agent for further studies in the search for therapeutic strategies to treat PSO in the future.

Narciclasine inhibits phospholipase A2 and regulates phospholipid metabolism to ameliorate psoriasis-like dermatitis

“…To identify the major targets of Ncs in alleviating skin immune cell infiltration and inflammation, we performed transcriptomic analysis of skin tissues from mice in the control group, Ncs group and IMQ group using RNA-seq ( Figure 4A ). Hierarchical clustering analysis of differentially expressed genes (DEGs) showed that compared with the control group, IMQ treatment up-regulated pathways related to keratinocyte differentiation and inflammation ( Figure S5 ), which was consistent with published studies ( 22 ). We further analyzed 558 DEGs (> 2-fold change) in the Ncs group versus the IMQ group and found that 230 were down-regulated due to Ncs treatment.…”

Neutrophil-Based Bionic Delivery System Breaks Through the Capillary Barrier of Liver Sinusoidal Endothelial Cells and Inhibits the Activation of Hepatic Stellate Cells

“…18 Studies demonstrated that baicalin (Bai) regulated immune-mediated chronic inflammatory signaling by targeting PPAR-γ. 19 In addition, Bai inhibited PDGF-BB-induced HSC activation and ameliorated LPS-induced HSCs migration in vitro. 20−22 Thus, Bai can be selected as an effective therapeutic agent against HSCs.…”

“…Activation of HSCs is intricately linked with the TGF-β1/Smad signaling pathway, wherein reduction of TGF-β1-induced Smad2/3 phosphorylation impedes HSC activation. , The TGF-β1/Smad signaling pathway was regulated by peroxisome proliferator-activated receptor-gamma (PPAR-γ), which had protective effects on hepatic fibrosis . Studies demonstrated that baicalin (Bai) regulated immune-mediated chronic inflammatory signaling by targeting PPAR-γ . In addition, Bai inhibited PDGF-BB-induced HSC activation and ameliorated LPS-induced HSCs migration in vitro . − Thus, Bai can be selected as an effective therapeutic agent against HSCs.…”

Combined baicalin-zinc hyaluronate treatment of psoriasis in mice

“…Baicalin ameliorates imiquimod (IMQ)induced skin damage, reduces in ammatory responses, and modulates immune disorders in mice. The underlying mechanism may be related to inhibition of the Wnt signaling pathway and inhibition of the Th17/IL-17 axis through activation of PPARγ [14]. However, the mechanism of action of baicalin on psoriasis requires further investigation.…”