Efficacy of Tanreqing Gel in Treating Acne and Its Effect on TLR2/MyD88/NF-κB Signaling Pathway
10.13422/j.cnki.syfjx.20260202
- VernacularTitle:痰热清凝胶治疗痤疮的药效探讨及其对TLR2/MyD88/NF-κB信号通路的影响
- Author:
Shuo YANG
1
;
Dongying LI
2
;
Yanan SUN
1
;
Yi WANG
1
Author Information
1. Experimental Research Center， China Academy of Chinese Medical Sciences， Beijing 100700， China
2. National Medical Products Administration Institute of Executive Development， Beijing 100073， China
- Publication Type:Journal Article
- Keywords:
Tanreqing gel;
acne;
Cutibacterium acnes;
Toll-like receptor 2 （TLR2）/myeloid differentiation 88 （MyD88）/nuclear factor-κB （NF-κB） signaling pathway;
anti-inflammatory mechanism
- From:
Chinese Journal of Experimental Traditional Medical Formulae
2026;32(20):102-111
- CountryChina
- Language:Chinese
-
Abstract:
ObjectiveTo explore the pharmacological mechanism of Tanreqing gel （TRQG） in the treatment of acne by regulating the Toll-like receptor 2 （TLR2）/myeloid differentiation 88 （MyD88）/nuclear factor-κB （NF-κB） signaling pathway. MethodsThe minimum inhibitory concentration （MIC） of Tanreqing injection （TRQ） against Cutibacterium acnes was determined through the microdilution broth method， and drug resistance induction experiments were conducted. A mouse model of acne was established through inoculation of C. acnes on the back. The effects of TRQG on skin structure， pustule formation， collagen repair， and inflammatory response were evaluated by dermoscopy， histopathology， two-photon excitation fluorescence microscopy （TPEF）， and optical coherence tomography （OCT）. Differentially expressed genes （DEGs） were identified through transcriptome sequencing and then subjected to KEGG pathway enrichment analysis. In the RAW264.7 cell model， the optimal dosage of TRQG was determined through cell viability assays. Subsequently， the expression of key proteins in the TLR2/MyD88/NF-κB pathway and downstream inflammatory factors ［tumor necrosis factor-α （TNF-α）， interleukin （IL）-1β， and IL-6］ was determined by Western blot and real-time PCR. ResultsThe MIC of TRQ against C. acnes was 4 125 mg·L-1. Although TRQ had weaker antibacterial activity than erythromycin （ERY） and fusidic acid （FA）， it was less likely to induce bacterial resistance. In vivo experiments showed that TRQG improved the skin structure， promoted collagen repair （P<0.01）， inhibited pustule formation （P<0.01）， alleviated follicular keratinization and sebaceous gland hyperplasia， and reduced inflammatory responses in the mouse model of acne compared with erythromycin gel （ERYG）. Transcriptome analysis suggested that the TLR/MyD88/NF-κB signaling pathway was a key enriched pathway. Further experimental validation indicated that TRQG inhibited the expression of TLR2， MyD88， TNF receptor-associated factor 6 （TRAF6）， phosphorylated （p）-transforming growth factor-β-activated kinase 1 （TAK1）， p-inhibitor of NF-κB subunit α （IκBα）， and p-NF-κB in this pathway （P<0.01）. Meanwhile， Real-time PCR results confirmed that TRQG reduced the mRNA levels of TNF-α， IL-1β， and IL-6 （P<0.01）. ConclusionTRQG exerts its therapeutic effect on acne by inhibiting the activation of the TLR2/MyD88/NF-κB signaling pathway and reducing the release of downstream inflammatory factors. Furthermore， it is less likely to induce bacterial resistance， indicating a promising application prospect.
