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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
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| 篇名： | 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 |
| TITLE： | Mechanisms of Qiaobai cold compress solution in improving acne vulgaris based on transcriptomics and experiment |
| 摘要： | 目的 基于转录组学和动物实验探究翘柏冷敷液（QBCS）改善寻常型痤疮（AV）的作用机制。方法将大鼠随机分为空白对照组（n＝6）和造模组（n＝30）。造模组大鼠以双耳内侧涂抹油酸联合耳廓皮下注射痤疮丙酸杆菌菌悬液的方式构建AV模型。将造模成功的大鼠分为模型组、阳性对照组（维A酸乳膏，0.045g/kg）和QBCS低、中、高剂量组[3.55、7.11、14.22g/kg（以生药量计）]，每组6只。各药物组大鼠涂抹相应药液，每天1次，连续14d。末次给药后，观察各组大鼠耳部外观形态、耳组织病理形态学变化情况，并检测其血清中炎症因子[肿瘤坏死因子α（TNF-α）、白细胞介素6（IL-6）、IL-1β]水平。收集空白对照组、模型组和QBCS中剂量组大鼠耳组织进行转录组测序，筛选差异表达基因（DEGs）并进行京都基因和基因组数据库通路富集分析，再运用实时荧光定量聚合酶链式反应、Westernblot实验进行验证。结果与模型组比较，QBCS各剂量组大鼠耳部痤疮症状均有所缓解，表皮增厚、皮脂腺增生、炎症细胞浸润等病理损伤有所减轻，血清中TNF-α（低剂量组除外）、IL-6（低剂量组除外）、IL-1β水平均显著降低（P＜0.05）。分别筛选出DEGs590个（空白对照组vs.模型组）、596个（模型组vs.QBCS中剂量组）；上述DEGs（空白对照组vs.模型组）主要富集于Toll样受体（TLR）、核因子κB（NF-κB）等信号通路。验证实验结果显示，与模型组比较，低、中、高剂量QBCS可不同程度地降低AV大鼠耳组织中TNF-α、TLR2、γ干扰素、CXC趋化因子配体8mRNA的表达水平，提高过氧化物酶体增殖物激活受体γ、肿瘤蛋白53mRNA的表达水平，并抑制NF-κBp65的磷酸化和TLR2、髓系分化初级反应蛋白88（MyD88）的表达（P＜0.05）。结论QBCS可缓解AV大鼠的耳部炎症及皮损；该作用可能与抑制TLR/MyD88/NF-κB信号通路，进而抑制TNF-α等下游相关炎症因子的表达有关。 |
| 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. |
| 期刊： | 2026年第37卷第04期 |
| 作者： | 谢圳江；朱维娜；曹亮亮；周芙琼；张淑盼；周柄文；陈寅生；李文；赵颖 |
| AUTHORS： | XIE Zhenjiang，ZHU Weina， CAO Liangliang，ZHOU Fuqiong，ZHANG Shupan，ZHOU Bingwen，CHEN Yinsheng，LI Wen，ZHAO Ying |
| 关键字： | 翘柏冷敷液；寻常型痤疮；转录组学；TLR/MyD88/NF-κB信号通路 |
| KEYWORDS： | Qiaobai cold compress solution； acne vulgaris； transcriptomics； TLR/MyD88/NF-κB signaling pathway |
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