Jianpi Yangxue Qufeng compound alleviates atopic dermatitis via TLR4/MyD88/NF-κB signaling pathway

Xuesong Yang; Zhimin Wang; Hong Huang; Guangyun Luo; Lin Cong; Jianting Yang; Jianzhou Ye

doi:10.1016/j.heliyon.2023.e23278

Jianpi Yangxue Qufeng compound alleviates atopic dermatitis via TLR4/MyD88/NF-κB signaling pathway

Heliyon. 2023 Dec 3;10(1):e23278. doi: 10.1016/j.heliyon.2023.e23278. eCollection 2024 Jan 15.

Authors

Xuesong Yang¹, Zhimin Wang¹, Hong Huang¹, Guangyun Luo², Lin Cong¹, Jianting Yang¹, Jianzhou Ye¹

Affiliations

¹ Department of Dermatology, First Affiliated Hospital of Yunnan University of Chinese Medicine, Kunming 650032, Yunnan, China.
² College of Basic Medicine, Yunnan University of Chinese Medicine, Kunming 650500, Yunnan, China.

Abstract

Background: Jianpi Yangxue Qufeng Compound (JPYXQFC) is a Chinese medicine widely used in the clinical treatment of atopic dermatitis (AD) and has a significantly therapeutic effect. However, the mechanism of JPYXQFC in AD has been not understood clearly.

Objective: This study aimed to explore the effect of JPYXQFC on AD model cells and rats by regulating TLR4/MyD88/NF-κB signaling pathway.

Methods: The rats (n > 5) were given JPYXQFC decoction orally twice a day for three days, and their abdominal aortic blood was collected. HaCaT cell proliferation rate was tested by cell counting kit-8 (CCK-8) assays. We induced AD rat model through 2, 4-dinitrofluorobenzene (DNFB). AD rats were given oral JPYXQFC decoction and cetirizine (positive control). HaCaT cells were pretreated with JPYXQFC drug serum or cetirizine for 0.5 h and then stimulated with TNF-α/IFN-γ for 1 h. The mRNA levels of TLR4, MyD88, NF-κB, IL-4, IL-13, MCP1, TNF-α and TSLP were detected by quantitative real-time PCR (Q-RT-PCR), and TLR4/MyD88/NF-κB pathway protein expression was tested by Western blot. The total serum levels of immunoglobulin E (IgE), thymus and activation regulated chemokine/chemokine (C-C motif) ligand 17 (TARC/CCL17) were detected by enzyme-linked immunosorbent assay (ELISA). The epidermal thickness was detected by hematoxylin and eosin (HE) staining. The dermatitis area and score were measured by a ruler and a four-point scoring method, respectively.

Results: JPYXQFC significantly inhibited mRNA and protein expression of the TLR4/MyD88/NF-κB pathway and Histone H3 in TNF-α/IFN-γ-induced HaCaT cells and DNFB-induced rats, decreased the mRNA of IL-4, IL-13, MCP1, CCL22, TSLP and the level of AD-related genes IgE and TAEC/CCL17 of TNF-α/IFN-γ-induced HaCaT cells. Meanwhile, JPYXQFC significantly reduced the dermatitis area and dermatitis score in DNFB-induced rats, inhibited the levels of pro-inflammatory cytokines IL-6 and TNF-α, and upregulated FLG, as well as inhibited the levels of IgE and TARC/CCL17 in the serum of AD rats.

Conclusion: JPYXQFC alleviates AD by inhibiting the activation of TLR4/MyD88/NF-κB pathway.

Keywords: Atopic dermatitis; Inflammation; TLR4/MyD88/NF-κB signaling pathway.