Mechanism of Shenqi guben formula in improving cancer-related fatigue by regulating IL-17 signaling pathway
- VernacularTitle: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
- Author:
Xin LI
1
;
Chongkai FANG
2
;
Yue HUANG
3
,
4
;
Yaoxuan LI
3
,
4
;
Haifu HUANG
3
,
4
;
Xianlin WU
3
;
Zhesheng CHEN
5
;
Meng LI
3
Author Information
1. Preventive Treatment of Disease Center，Shenzhen Hospital （Futian） of Guangzhou University of Chinese Medicine，Guangdong Shenzhen 518034，China
2. Science and Technology Innovation Center，Guangzhou University of Chinese Medicine，Guangzhou 510405，China
3. Shenzhen Traditional Chinese Medicine Oncology Medical Center，Guangdong Shenzhen 518034，China
4. Dept. of Oncology，Shenzhen Hospital （Futian） of Guangzhou University of Chinese Medicine，Guangdong Shenzhen 518034，China
5. St. John’s University，New York 11439，USA
- Publication Type:Journal Article
- Keywords:
Shenqi guben formula;
network pharmacology;
cancer-related fatigue;
cellular experiments
- From:
China Pharmacy
2025;36(14):1722-1729
- CountryChina
- Language:Chinese
-
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.
