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参芪固本方调控IL-17信号通路改善癌因性疲乏的作用机制
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| 篇名： | 参芪固本方调控IL-17信号通路改善癌因性疲乏的作用机制 |
| TITLE： | Mechanism of Shenqi guben formula in improving cancer-related fatigue by regulating IL-17 signaling pathway |
| 摘要： | 目的 基于网络药理学和细胞实验探讨参芪固本方改善癌因性疲乏（CRF）的作用机制。方法基于TCMSP等数据库挖掘参芪固本方活性成分及CRF相关靶点，并进行富集分析。采用白细胞介素17（IL-17）诱导A549细胞建立CRF细胞模型，使用低（1.0mg/mL）、高质量浓度（1.5mg/mL）参芪固本方干预，通过细胞划痕实验、流式细胞术、酶联免疫吸附测定、实时荧光定量聚合酶链式反应实验及Westernblot等方法验证其对细胞活力、迁移、凋亡、炎症因子及其mRNA表达、凋亡相关蛋白和IL-17信号通路关键蛋白的影响。结果共得到84个活性成分及209个CRF交集靶点，其中槲皮素、山柰酚和木犀草素等为核心活性成分，肿瘤蛋白p53、丝氨酸/苏氨酸激酶1、IL-6、肿瘤坏死因子（TNF）等为核心靶点，IL-17、TNF、磷脂酰肌醇3激酶/蛋白激酶B信号通路为关键通路。与IL-17干预组比较，IL-17+参芪固本方低、高质量浓度组细胞的迁移率，B淋巴细胞瘤2（Bcl-2）蛋白表达，上清液中IL-6、TNF-α水平，IL-17受体A（IL-17RA）、IL-6、TNF-αmRNA表达，IL-17RA、核因子κBp65亚基（p65）蛋白表达和磷酸化p65（p-p65）/p65比值均显著降低或下调（P＜0.05）；凋亡率，Bcl-2相关X蛋白（Bax）、切割型胱天蛋白酶3蛋白表达、Bax/Bcl-2比值，磷酸化p38丝裂原活化的蛋白激酶（p-p38MAPK）蛋白表达、p-p38MAPK/p38MAPK比值均显著升高或上调（P＜0.05）；且高质量浓度组上述指标的改善大多优于低质量浓度组（P＜0.05）。结论参芪固本方可能通过调控IL-17信号通路、抑制炎症因子表达、激活p38MAPK依赖的凋亡过程来改善CRF。 |
| ABSTRACT： | OBJECTIVE To explore the mechanism of Shenqi guben formula （SQGB） in improving cancer-related fatigue （CRF） based on network pharmacology and cellular experiments. METHODS Active components of SQGB and CRF-related targets were identified on the basis of databases such as the Traditional Chinese Medicine Systems Pharmacology platform. An in vitro CRF cell model was established by inducing A549 cells with interleukin-17 （IL-17）. Cells were treated with low （1.0 mg/mL） or high （1.5 mg/mL） concentrations of SQGB. The effects on cell viability， migration， apoptosis， inflammatory factors， mRNA expression， apoptosis-related proteins and key proteins 011） of IL-17 signaling pathway were evaluated using scratch assay， flow cytometry， ELISA， real-time fluorescent quantitative PCR and Western blot analysis. RESULTS SQGB contained 84 active components acting on 209 potential CRF targets. Among E-these， quercetin， kaempferol， and luteolin were identified as the core components of the compound. Core targets included tumor protein p53， AKT serine/threonine kinase 1， IL-6， and tumor necrosis factor （TNF）. IL-17， TNF and phosphatidylinositol-3- kinase-serine/threonine protein kinase （PI3K/Akt） signaling pathways were identified as crucial pathways. Compared with IL-17 intervention group， the cell migration rate， B-cell lymphoma 2 （Bcl-2） protein expression， the levels of IL-6 and TNF-α in the supernatant， mRNA expression of IL-17 receptor A （IL-17RA）， TNF-α， and IL-6， as well as the protein expression of IL-17RA and nuclear factor kappa-B p65 subunit （p65）， and phosphorylated （p）-p65/p65 ratio in IL-17+SQGB low- and high- quality concentration groups were all significantly decreased or down-regulation （P＜0.05）； the apoptosis rate， expression levels of Bcl-2 associated X protein （Bax） and cleaved caspase-3 protein， the ratio of Bax/Bcl-2， the expression level of p-p38 protein， and the p- p38/p38 ratio were all significantly increased or up-regulated （P＜0.05）. Moreover， the improvement effects of these indicators were mostly better in the high-quality concentration groups compared to the low-quality concentration groups （P＜0.05）. CONCLUSIONS SQGB ameliorates CRF by regulating the IL-17 signaling pathway， inhibiting the expression of inflammatory factors， and activating p38 MAPK-dependent apoptosis pathway. |
| 期刊： | 2025年第36卷第14期 |
| 作者： | 李鑫；方崇锴；黄越；李要轩；黄海福；吴先林；CHENZhesheng；李萌 |
| AUTHORS： | LI Xin，FANG Chongkai，HUANG Yue，LI Yaoxuan，HUANG Haifu，WU Xianlin，CHEN Zhesheng，LI Meng |
| 关键字： | 参芪固本方；网络药理学；癌因性疲乏；细胞实验 |
| KEYWORDS： | Shenqi guben formula； network pharmacology； cancer-related fatigue； cellular experiments |
| 阅读数： | 11 次 |
| 本月下载数： | 1 次 |
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