Sanjie Quban Prescription Affects Proliferation， Apoptosis， Migration， and Invasion of Human Keloid Fibroblasts via AhR/CYP1A1 Signaling Pathway
10.13422/j.cnki.syfjx.20251806
- VernacularTitle:基于AhR/CYP1A1信号通路探讨散结祛瘢方对人瘢痕疙瘩成纤维细胞增殖、凋亡、迁移及侵袭能力的影响
- Author:
Zhihong HE
1
;
Fengchuan ZHANG
2
;
Dingquan YANG
3
;
Chuhan HUANG
1
;
Zhihan WANG
1
;
Yatong WU
3
;
Qingwu LIU
3
Author Information
1. Beijing University of Chinese Medicine， Beijing 100029， China
2. Dongfang Hospital of Beijing University of Chinese Medicine， Beijing 100078， China
3. National Center for Integrated Traditional Chinese and Western Medicine， China-Japan Friendship Hospital， Beijing 100029， China
- Publication Type:Journal Article
- Keywords:
Sanjie Quban prescription;
aryl hydrocarbon receptor （AhR）/cytochrome P450 family 1 subfamily A member 1 （CYP1A1） signaling pathway;
keloid;
fibroblast
- From:
Chinese Journal of Experimental Traditional Medical Formulae
2026;32(17):164-174
- CountryChina
- Language:Chinese
-
Abstract:
ObjectiveTo investigate the effects of Sanjie Quban prescription （SJQB）-containing serum on the proliferation， apoptosis， migration， and invasion of human keloid fibroblasts （KFs） and to elucidate its underlying mechanism， with a focus on the aryl hydrocarbon receptor （AhR）/cytochrome P450 family 1 subfamily A member 1 （CYP1A1） signaling pathway. MethodsPrimary human KFs were cultured in vitro and assigned to the following groups： control （KFs+blank serum）， asiaticoside （KFs+asiaticoside-containing serum）， SJQB （KFs+SJQB-containing serum）， AhR agonist （KFs+β-naphthoflavone）， AhR inhibitor （KFs+CH223191）， and AhR inhibitor+SJQB （KFs+CH223191+SJQB-containing serum）. The optimal intervention concentrations were determined through the cell counting kit-8 （CCK-8） assay. Cell proliferation， apoptosis， migration， and invasion were evaluated by the EdU assay， flow cytometry， wound healing assay， and Transwell assay， respectively. The expression of transforming growth factor-β1 （TGF-β1） and α-smooth muscle actin （α-SMA） was visualized by immunofluorescence. The mRNA and protein levels of AhR， CYP1A1， TGF-β1， and α-SMA were measured by Real-time fluorescence quantitative polymerase chain reaction （Real-time PCR） and Western blot， respectively. ResultsCompared with the control group， the SJQB， asiaticoside， and AhR agonist groups demonstrated inhibited cell proliferation， migration， and invasion， along with an increased apoptosis rate （P<0.01）. The AhR inhibitor group showed enhanced proliferation， migration， and invasion together with a reduced apoptosis rate in comparison with the AhR agonist group （P<0.01）. The AhR inhibitor+SJQB group exhibited increased proliferation， migration， and invasion as well as decreased apoptosis compared with the SJQB group （P<0.05， P<0.01）. At the molecular level， compared with the control group， the SJQB， asiaticoside， and AhR agonist groups presented upregulated protein and mRNA levels of AhR and CYP1A1 （P<0.05， P<0.01）， while the SJQB and AhR agonist groups showed downregulated TGF-β1 and α-SMA expression at both protein and mRNA levels （P<0.05， P<0.01）， and the asiaticoside group displayed decreased protein level of TGF-β1 and mRNA level of α-SMA （P<0.05， P<0.01）. Compared with both the AhR agonist and control groups， the AhR inhibitor group exhibited decreased AhR and CYP1A1 expression but increased TGF-β1 and α-SMA expression at protein and mRNA levels （P<0.01）. In comparison with the SJQB group， the AhR inhibitor+SJQB group demonstrated reduced AhR and CYP1A1 expression （P<0.01） and elevated TGF-β1 and α-SMA expression （P<0.05， P<0.01） at both protein and mRNA levels. ConclusionSJQB may activate the AhR/CYP1A1 signaling pathway to downregulate TGF-β1 and α-SMA expression， thereby suppressing the proliferation， migration， and invasion and inducing the apoptosis of KFs.
