Mechanism of Xiezhuo Huayu Yiqi Tongluo Formula in the Treatment of Uric Acid Nephropathy Based on Network Pharmacology, Molecular Docking, and In Vivo Experiments

Fan, Lifei; Guo, Yuqin; Wu, Qianni; Hu, Tingting; Chen, Xiaomei; Guo, Jun; Liu, Ying; Lu, Yuhui; Lin, Min

doi:10.1155/2023/6931644

Cited by 7 publications

(6 citation statements)

References 27 publications

(28 reference statements)

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“…Furthermore, investigations into specific compounds, such as kaempferol and quercetin, suggest their role in modulating PPARG expression and interacting with AKT1, pointing towards potential treatment avenues for endometrial cancer and nonsegmental vitiligo [ 22 , 23 ]. The relevance of these interactions extends to conditions like uric acid nephropathy, pneumonia, and type 2 diabetes mellitus, as demonstrated by studies using Xiezhuo Huayu Yiqi Tongluo Formula (XHYTF), Fritillariae thunbergii bulbus, and Alpinia officinarum Hance [ 24 – 26 ].…”

Section: Discussionmentioning

confidence: 99%

PPARG and the PTEN-PI3K/AKT Signaling Axis May Cofunction in Promoting Chemosensitivity in Hypopharyngeal Squamous Cell Carcinoma

Han,

Chen,

Chen

et al. 2024

PPAR Research

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It has been demonstrated that PPARG may interact with the PTEN-PI3K/AKT pathway, contributing to its involvement in the chemotherapy treatment of hypopharyngeal squamous cell carcinoma (HSCC). However, the underlying mechanism remains largely unknown. In this study, gene expression profiles of 17 HSCC patients, comprising 8 chemotherapy-sensitive patients (CSP) and 9 chemotherapy-nonsensitive patients (CNSP), were collected and analyzed to investigate expression patterns, correlations, influencing factors of the PPARG-PTEN-PI3K/AKT pathway, and its role in regulating chemosensitivity. The results revealed significantly increased expression (p<0.04) of AKT1, AKT2, AKT3, PIK3CA, PPARG, and PTEN in the CSP group compared to the CNSP group. Specifically, AKT2 exhibited significant overexpression in tumor tissue (p=0.01), while AKT2, AKT3, PPARG, and PTEN displayed significant increases in normal tissue (p≤0.04). Positive correlations (R∈0.43,0.71, p<0.014) were observed between PIK3CA, AKT1, AKT2, AKT3, and PTEN, with AKT2, AKT3, and PTEN also showing significant correlations with PPARG (R∈0.35,0.47, p<0.04). Age, gender, and disease stage had no influence on PPARG, PIK3CA, and PTEN expression, but they may affect AKT expressions. Pathway analysis revealed that PPARG may interact with the PTEN-PI3K/AKT signaling pathway, playing a crucial role in regulating chemosensitivity in the normal tissue microenvironment. Our results suggest that AKT1 and PIK3CA may be associated with chemosensitivity in HSCC tumor cells, while PPARG and PTEN might exhibit a correlation with a specific segment of the PI3K/AKT pathway, potentially influencing chemosensitivity in the normal tissue microenvironment of HSCC patients.

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Section: Discussionmentioning

confidence: 99%

PPARG and the PTEN-PI3K/AKT Signaling Axis May Cofunction in Promoting Chemosensitivity in Hypopharyngeal Squamous Cell Carcinoma

Han,

Chen,

Chen

et al. 2024

PPAR Research

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“…The molecular docking was used to simulate the interaction of quercetin and XOD referring to Fan et al (2023). The crystal structure corresponding to core targets of XOD was obtained from the website of http://www.rcsb.org and the ligand molecule of quercetin was obtained from http://www.pubchem.ncbi.nlm.nih.gov.…”

Section: Methodsmentioning

confidence: 99%

Section: Molecular Docking and Fluorescence Spectroscopy Assaymentioning

confidence: 99%

Quercetin ameliorates hyperuricemic nephropathy by repressing uric acid synthesis and reabsorption in mice and cells

Li,

Chen,

et al. 2024

eFood

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Hyperuricemia as one of the key factors for gout, and quercetin could reduce the uric acid (UA) content. However, the mechanism of quercetin reduces UA content is still uncovered. Herein, we found quercetin can reduce UA content, induce antioxidant enzyme activity, inhibit the enzyme activity of xanthine oxidase (XOD) in hyperuricemia mice. Moreover, the UA reabsorption was also significantly reduced in the kidney and the kidney inflammation was alleviated by quercetin in hyperuricemia mice. Meanwhile, the protein level of ATP‐binding cassette super‐family G member 2 (ABCG2) was markedly induced and the protein levels of urate transporter 1 (URAT1) and glucose transporter 9 (GLUT9) were significantly repressed by quercetin in hyperuricemia mice and HK‐2 cells and by quercetin‐3‐O‐glucuronide in HK‐2 cells. Additionally, the docking mode indicated that quercetin is stable bound to the active site of XOD. Overall, the data reveal that quercetin alleviates hyperuricemia by repressing the activity of XOD, reducing the UA absorption via enhancing ABCG2 expression, and repressing URAT1 and GLUT9 expression.

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“…Network pharmacology is a rapidly evolving field of research that aims to unravel the intricacies of disease and drug mechanisms within complex biological networks [ 7 ]. This approach has revolutionized investigations by providing a systematic framework to address scientific challenges at multiple levels.…”

Section: Introductionmentioning

confidence: 99%

Network pharmacology-based strategy to investigate the effect and mechanism of α-solanine against glioma

Wang,

Liu,

Guo

2023

BMC Complement Med Ther

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Background An anti-tumour activity has been demonstrated for α-solanine, a bioactive compound extracted from the traditional Chinese herb Solanum nigrum L. However, its efficacy in the treatment of gliomas and the underlying mechanisms remain unclear. The aim of this study was to investigate the inhibitory effects of α-solanine on glioma and elucidate its mechanisms and targets using network pharmacology, molecular docking, and molecular biology experiments. Methods Traditional Chinese Medicine Systems Pharmacology Database and Analysis Platform (TCMSP) was utilized to predict the potential targets of α-solanine. GeneCards was used to gather glioma-related targets, and the STRING online database was used to analyze protein–protein interaction (PPI) networks for the shared targets. Hub genes were identified from the resulting PPI network and further investigated using Gene Ontology (GO) enrichment and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis. Additionally, prognostic and gene set enrichment analyses (GSEA) were carried out to identify potential therapeutic targets and their underlying mechanisms of action in relation to the prognosis of gliomas. In vitro experiments were conducted to verify the findings from the network pharmacology analysis. Results A total of 289 α-solanine targets and 1149 glioma-related targets were screened, of which 78 were common targets. 11 hub genes were obtained, including SRC, HRAS, HSP90AA1, IGF1, MAPK1, MAPK14, KDR, STAT1, JAK2, MAP2K1, and IGF1R. The GO and KEGG pathway analyses unveiled that α-solanine was strongly associated with several signaling pathways, including positive regulation of MAP kinase activity and PI3K-Akt. Moreover, α-solanine (10 µM and 15 µM) inhibited the proliferation and migration but promoted the apoptosis of glioma cells. Finally, STAT1 was identified as a potential mediator of the effect of α-solanine on glioma prognosis. Conclusion α-Solanine can inhibit the proliferation and migration of gliomas by regulating multiple targets and signalling pathways. These findings lay the foundation for the creation of innovative clinical anti-glioma agents.

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Mechanism of Xiezhuo Huayu Yiqi Tongluo Formula in the Treatment of Uric Acid Nephropathy Based on Network Pharmacology, Molecular Docking, and In Vivo Experiments

Cited by 7 publications

References 27 publications

PPARG and the PTEN-PI3K/AKT Signaling Axis May Cofunction in Promoting Chemosensitivity in Hypopharyngeal Squamous Cell Carcinoma

PPARG and the PTEN-PI3K/AKT Signaling Axis May Cofunction in Promoting Chemosensitivity in Hypopharyngeal Squamous Cell Carcinoma

Quercetin ameliorates hyperuricemic nephropathy by repressing uric acid synthesis and reabsorption in mice and cells

Network pharmacology-based strategy to investigate the effect and mechanism of α-solanine against glioma

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