Mechanisms of Qiaobai cold compress solution in improving acne vulgaris based on transcriptomics and experiment
- VernacularTitle:基于转录组学和实验验证的翘柏冷敷液改善寻常型痤疮的机制
- Author:
Zhenjiang XIE
1
;
Weina ZHU
2
;
Liangliang CAO
1
;
Fuqiong ZHOU
2
;
Shupan ZHANG
1
;
Bingwen ZHOU
3
;
Yinsheng CHEN
4
;
Wen LI
5
;
Ying ZHAO
1
Author Information
1. Dept. of Pharmacy，Nanjing Hospital of Chinese Medicine Affiliated to Nanjing University of Chinese Medicine，Nanjing 210022，China
2. Medical Experimental Centre，Nanjing Hospital of Chinese Medicine Affiliated to Nanjing University of Chinese Medicine，Nanjing 210022，China
3. Jiangsu Provincial Clinical Medical Innovation Center for Anorectal Diseases of Traditional Chinese Medicine，Nanjing Hospital of Chinese Medicine Affiliated to Nanjing University of Chinese Medicine，Nanjing 210022，China
4. Institute of Traditional Chinese Medicine，Nanjing Hospital of Chinese Medicine Affiliated to Nanjing University of Chinese Medicine，Nanjing 210022，China
5. Clinical Trial Institution，Nanjing Hospital of Chinese Medicine Affiliated to Nanjing University of Chinese Medicine，Nanjing 210022，China
- Publication Type:Journal Article
- Keywords:
Qiaobai cold compress solution;
acne vulgaris;
transcriptomics;
TLR/MyD88/NF-κB signaling pathway
- From:
China Pharmacy
2026;37(4):425-430
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVE To investigate the mechanism by which Qiaobai cold compress solution （QBCS） improves acne vulgaris （AV） based on transcriptomics and animal experiments. METHODS Rats were randomly divided into a blank control group （ n ＝6） and a modeling group （ n ＝30）. AV models were established in the modeling group by topical application of oleic acid to the inner surface of both ears， combined with subcutaneous injection of Cutibacterium acnes suspension into the auricle. Successfully modeled rats were further divided into the model group， positive control group （Tretinoin cream， 0.045 g/kg）， and QBCS low-， medium-， high-dose groups [3.55， 7.11， 14.22 g/kg （calculated by the amount of crude drug） ] ， with 6 rats in each group. Rats in each d rug group were treated with the corresponding drugs once daily for 14 consecutive days. After the final administration， changes in the appearance of the ears and histopathological changes in the ear tissues were observed， and serum levels of inflammatory factors， including tumor necrosis factor-α （TNF-α）， interleukin-6 （IL-6） and IL-1β， were measured. Auricular tissues from the blank control group， model group and QBCS medium-dose group were collected for transcriptome sequencing. Differential expressed genes （DEGs） were screened and subjected to Kyoto Encyclopedia of Genes and Genomes pathway enrichment analysis， followed by validation using real-time quantitative polymerase chain reaction and Western blot assay. RESULTS Compared with the model group， rats in all QBCS groups showed alleviated auricular acne symptoms， with reduced epidermal thickening， sebaceous gland hyperplasia， and inflammatory cell infiltration. Serum levels of TNF-α （except for the QBCS low-dose group）， IL-6 （except for the QBCS low-dose group） and IL-1β were significantly decreased （ P ＜0.05）. A total of 590 DEGs were identified （blank control group vs. model group）， and 596 DEGs were identified （model group vs. QBCS medium-dose group）. Above DEGs （blank control group vs. model group） were mainly enriched in Toll-like receptor （TLR） and nuclear factor-kappa B （NF-κB） signaling pathways， etc. Validation experiments showed that， compared with model group， low-， medium- and high-dose of QBCS reduced， to varying degrees， the mRNA expression of TNF-α， TLR2， interferon-γ and CXC chemokine ligand 8 in the auricular tissues of AV rats， increased the mRNA expression of peroxisome-proliferator-activated receptor gamma and tumor protein 53， and inhibited the phosphorylation of NF-κB p65 protein as well as the expressions of TLR2 and myeloid differentiation primary response protein 88（MyD88） （ P ＜0.05）. CONCLUSIONS QBCS can alleviate auricular inflammation and skin lesions in AV rats. This effect may be related to inhibition of the TLR/MyD88/NF-κB signaling pathway， thereby suppressing the expression of downstream inflammatory factors such as TNF-α.
