Core Targets Research Articles

Potential Molecular Mechanism of Bajitian-Niuxi Formula Delays Intervertebral Disc Degeneration: An Animal Experiment and Network Pharmacology.

Intervertebral disc degeneration (IDD) continues to be a major health concern. The combination of Bajitian and Niuxi (B&N) is commonly used to treat musculoskeletal degenerative diseases. This study aimed to explore the potential of B&N in treating IDD through in vivo experiments and bioinformatics approaches. Through in vivo experiments, it was found that the process of IDD in rats treated with B&N extracts was delayed. Through database screening and network pharmacology analysis, it was discovered that multiple key drug active ingredients (DAIs) of B&N, such as Wogonin, Baicalein, 1-hydroxy-3-methoxy-9,10-anthraquinone, and β-sitosterol, might play a role in the treatment of IDD, among which signaling pathways such as PI3K-AKT, MAPK and senescence signaling might be the main drug-regulated pathways. The binding potential and position of the main DAIs to the core targets were verified by structural bioinformatics. Immunohistochemistry and qRT-PCR results indicated that B&N treatment could improve the expressions of Col-2 and ANCA in IDD rats, which might be related to the phosphorylation levels of AKT and p38. Therefore, the B&N formula might delay IDD in rats by regulating multiple signaling pathways through DAIs, which provides new approaches for further exploring the prevention and treatment strategies of IDD with traditional Chinese medicine.

Zearalenone (ZEN) impairs motor function and induces neurotoxicity via inflammatory pathways: Evidence from zebrafish models and molecular docking studies.

Zearalenone (ZEN) impairs motor function and induces neurotoxicity via inflammatory pathways: Evidence from zebrafish models and molecular docking studies.

Tetrahydrocurcumin-induced apoptosis of hepatocellular carcinoma cells involves the TP53 signaling pathway, as determined by network pharmacology.

Hepatocellular carcinoma (HCC) is a malignant disease with high incidence and mortality worldwide. This study focuses on the TP53 target protein to investigate the potential therapeutic effect of tetrahydrocurcumin (THC) on HCC and its mechanism of action. The research hypothesis is that THC can inhibit the proliferation, migration, and invasion of HCC cells, and promote their apoptosis by regulating the TP53 target protein. To explore the mechanism by which THC inhibits HCC cell proliferation via the TP53 signaling pathway. Potential targets of THC and HCC were identified from multiple databases. The core targets were subjected to analyses using Gene Ontology and Kyoto Encyclopedia of Genes and Genomes databases, and visualization processing, using the online platform Metascape to identify the key molecules and signaling pathways involved in the action of THC against HCC. The molecular mechanisms of action of THC against TP53 in the inhibition of HCC cells were verified using cell counting kit-8, Transwell, apoptosis, and western blotting assays. Molecular docking results showed that THC had a high score for the TP53 target protein. In vitro experiments indicated that THC effectively inhibited the proliferation and migration of HCC cells, and affected the expression levels of TP53, MDM2, cyclin B, Bax, Bcl-2, caspase-9, and caspase-3. THC induces the apoptosis of HCC cells through the TP53 signaling pathway, thereby inhibiting their proliferation and migration.

Exploring the mechanism of vitamin C on the co-expressed genes of papillary thyroid carcinoma and Epstein-Barr virus based on bioinformatics, network pharmacology and molecular docking analysis

ObjectiveThe study aims to evaluate the role and mechanism of action of vitamin C as an anti- Epstein-Barr virus (EBV) and papillary thyroid carcinoma (PTC) therapeutic agent.MethodsThe PTC/EBV-associated genes were obtained by intersection and further screen out hub genes to construct a prognostic model. The relationship between PTC/EBV-related genes and core genes and immune infiltration was analyzed, respectively. Finally, the core targets of vitamin C against PTC/EBV were screened, and the binding sites were determined by molecular docking with vitamin C.ResultsThe diagnostic efficiency and prognostic value of this model was good. The prognostic model performed well in male, female, classical, T3-4, N0, and N1 subgroups. Core genes STAT1 and APOE were highly expressed and FGF7 was lowly expressed in PTC. The core genes STAT1, APOE and FGF7 were significantly correlated with a variety of immune cells. 263 vitamin C-related targets were screened by the database, and 11 cross genes between vitamin C and PTC/EBV were identified. 4 molecular targets with the best performance, LGALS3, MMP9, CTSB and CTSS, were identified by topological analysis, and the binding energies were all < -5.0 kcal/mol.ConclusionsOur prognostic model has good diagnostic and prognostic effects and has potential value of basic research. This study for the first time revealed the related molecular functions of vitamin C and the molecular targets for the treatment of PTC/EBV.

Network pharmacology and in vitro experiments based strategy to explore the effects of Jujuboside A on the proliferation and migration ability of glioma cells.

Network pharmacology and in vitro experiments based strategy to explore the effects of Jujuboside A on the proliferation and migration ability of glioma cells.

Whole transcriptome analysis in oviduct provides insight into microRNAs and ceRNA regulative networks that targeted reproduction of goat (Capra hircus)

BackgroundReproduction traits are crucial for livestock breeding and represent key economic indicators in the domestic goat (Capra hircus) industry. The oviduct, a critical organ in female mammals, plays a pivotal role in several reproductive processes; however, its molecular mechanisms remain largely unknown. Non-coding RNA and mRNAs are essential regulatory elements in reproductive processes; yet their specific roles and regulatory networks in goat oviducts remain unclear.ResultsIn this study, we conducted small RNA sequencing of the oviduct in high- and low-fecundity goats during the follicular (FH and FL groups, n = 10) and luteal (LH and LL groups, n = 10) phase, profiling 20 tissue samples. Combinatorial whole-transcriptome expression profiles were applied to the same samples to uncover the competitive endogenous RNA (ceRNA) regulation network associated with goat fecundity. RT-qPCR was employed to validate the miRNA profiling results, and ceRNA regulatory networks were analyzed through luciferase assay. Gene set enrichment analysis (GSEA) confirmed that the cytokine-cytokine receptor interaction and TGF-β signaling pathway, both related to embryonic development, were enriched in DEM target genes. Additionally, miR-328-3p, a core miRNA, targets SMAD3 and BOP1, which are involved in the negative regulation of cell growth and embryonic development. TOB1 and TOB2, targeted by miR-204-3p, regulate cell proliferation via the protein kinase C-activating G-protein coupled receptor signaling pathway. Analyses of ceRNA regulatory networks revealed that LNC_005981 − miR-328-3p − SMAD3 and circ_0021923 − miR-204-3p − DOT1L may affect goats’ reproduction, findings that were validated using luciferase assay.ConclusionAnalysis of whole-transcriptome profiling of goat oviducts identified several key miRNAs and ceRNAs that may regulate oocyte maturation, embryo development, and the interactions between the oviduct and gametes/early embryos, providing insights into the molecular mechanisms of reproductive regulatory networks.

Cell-free supernatant of Clostridium leptum inhibits breast cancer cell proliferation.

Breast cancer has emerged as the leading cause of global cancer incidence, surpassing lung cancer. Accumulating evidence suggests that probiotics exhibit inhibitory effect on breast cancer progression, highlighting the need to identify gut flora-derived probiotics with potential anti-breast cancer properties. Here, we investigated the effect of the cell-free supernatant of C. leptum (ClCFS) on breast cancer cells by MTT assay. Untargeted metabolomics analysis was employed to characterize metabolite alterations in ClCFS. Furthermore, the core targets were predicted by the protein-protein interaction network and the signaling pathways were enriched by the Kyoto Encyclopedia of Genes and Genomes analysis. Our findings demonstrated that ClCFS inhibited the proliferation of breast cancer cells and that the main metabolite of ClCFS might be acetylcarnitine. Utilizing network pharmacological analysis, we identified apoptosis-related signaling pathways as the principal mechanisms underlying ClCFS activity. Furthermore, five core targets of STAT3, IL-1β, BCL2, CASP3, and ESR1 were identified. This study elucidates the main bioactive constituent and the potential targets of ClCFS against breast cancer. It provides a new understanding of the pharmacological activity of ClCFS in breast cancer treatment.

Identification of bioactive compounds and molecular targets of Fuke Huahuang formulation to treat vaginitis.

Fuke Huahuang formulation (FHF) is widely used in the treatment of vaginitis, with clinical evidence indicating its promising anti-inflammatory properties. We explored the bioactive components and potential mechanisms of FHF for treating vaginitis, and reveal its pharmacological activities against vaginitis. A total of 12 anti-inflammatory components in FHF and 584 pharmacological targets were identified. Furthermore, 1427 vaginitis-associated targets were identified, and 184 intersection targets between FHF and vaginitis were constructed for network analysis. Gene Ontology and pathway analysis revealed that the therapeutical targets of FHF against vaginitis are involved in modulating inflammatory stress, enhancing immunoregulation, reconstructing the microenvironment, and suppressing cell damage. Molecular docking analysis further suggested the possible direct binding of the bioactive compounds of FHF (fumarine) to the core targets, including AKT Serine/Threonine Kinase 1 (AKT1), Signal Transducer and Activator of Transcription 3 (STAT3), and nuclear factor-kappaB (NF-κB). Experimental validation found that FHF-treated vaginitis rats exhibited reduced intracellular AKT1, STAT3, and NF-κB protein expressions. Overall, we identified the bioactive compounds and pharmacological mechanisms of FHF against vaginitis, thus offering a theoretical fundament for exploring FHF for treating vaginitis in the future.

Network pharmacological approach combined with weighted gene co-expression network analysis identifies CDKN2A as the keg target of Changweiqing against colorectal cancer

Background and objectiveChangweiqing (CWQ) is a Chinese herbal formula for the treatment of the gastrointestinal tract diseases, but its role in the treatment of colorectal cancer (CRC) has not been clarified. This study aimed to explore the molecular mechanism of CWQ in CRC treatment through bioinformatics analysis and network pharmacology.MethodsTraditional Chinese Medicine Systems Pharmacology Database and Analysis Platform and SwissTargetPrediction database were used to collect the bioactive components of CWQ. The databases including DisgeNET, GeneCards, MalaCards, Online Mendelian Inheritance in Man and Comparative Toxicogenomics were used to obtain CRC-related targets. The Cancer Genome Atlas - colon adenocarcinoma dataset was used to obtain prognosis-related genes in CRC based on weighted gene co-expression network analysis (WGCNA). A protein-protein interaction network was constructed to screen core targets, with STRING database and Cytoscape software. Gene Ontology and Kyoto Encyclopedia of Genes and Genomes enrichment analyses were performed using the Database for Annotation, Visualization and Integrated Discovery database. Molecular docking was performed with AutoDock Vina software. Core targets were further analyzed using Gene Expression Profiling Interactive Analysis platform, Human Protein Atlas database, University of ALabama at Birmingham CANcer data analysis Portal (UALCAN) and GeneMANIA database. In vitro experiments were further performed to investigate the effects of quercetin, one of the main components of CWQ, on CRC cells.Results6356, 1901 and 2980 CRC-related genes were obtained from differential expression analysis, WGCNA and open access databases, respectively. CWQ contained a total of 70 bioactive ingredients, of which 64 ingredients had a total of 836 therapeutic targets. Functional enrichment analysis indicated that CWQ may be involved in regulating pathways in cancer, MAPK signaling pathway and AGE-RAGE signaling pathway, and further analysis identified 14 core targets of CWQ. These core targets were significantly correlated with cell cycle, p53 signaling pathway, FoxO signaling pathway and pathways in cancer. Among these core targets, cyclin-dependent kinase inhibitor 2 A (CDKN2A) expression was closely associated with shorter overall survival and clinical stage of CRC patients. The main bioactive ingredients of CWQ targeting CDKN2A were quercetin, luteolin, kaempferol, isorhamnetin, 7-O-methylisomucronulatol and 7-Methoxy-2-methyl isoflavone. Additionally, quercetin caused G0/G1 phase arrest and inhibited the viability of CRC cells.ConclusionThe active ingredients of CWQ may play an anti-CRC role through multi-targets and multi-pathways, regulating the cell cycle and cell viability of CRC cells.

Analysis of the mechanism of Eleutherococcus senticosus inducing ferroptosis in the treatment of gastric cancer by integrating network pharmacology, transcriptome, and metabolomics

Analysis of the mechanism of <i>Eleutherococcus senticosus</i> inducing ferroptosis in the treatment of gastric cancer by integrating network pharmacology, transcriptome, and metabolomics

Huoshan Dendrobium Zengye Jiedu Formula mitigates radiation-induced oral mucositis and improves oral immune microenvironment by targeting the EGFR/PI3K/AKT pathway: evidence from network pharmacology, molecular docking, and experimental validation

IntroductionRadiation-induced oral mucositis (RIOM) manifests as mucosal ulceration, pain, and dysphagia, disrupting treatment and quality of life. Its pathogenesis involves inflammatory imbalance and immune dysregulation, driven by microbial infiltration and cytokine storms. Current therapies remain inadequate, necessitating deeper exploration of immune-microbial interactions for effective interventions.MethodsBioactive components of Huoshan Dendrobium Zengye Jiedu Formula (HDZJF) and RIOM-related targets were retrieved from public databases. Core therapeutic targets and pathways were systematically analyzed via protein-protein interaction (PPI) networks, Gene Ontology (GO), and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment. Molecular docking evaluated interactions between HDZJF components and key targets. A rat RIOM model validated HDZJF efficacy by assessing mucositis severity, inflammatory cytokines, and EGFR/PI3K/AKT pathway protein expression.ResultsA total of 102 bioactive components and 379 potential targets for RIOM were identified. GO and KEGG enrichment analyses suggest that HDZJF exerts therapeutic effects on RIOM by modulating processes such as angiogenesis, inflammation, and apoptosis through pathways like PI3K-AKT. Molecular docking confirmed strong binding affinities between HDZJF components and key targets. In vivo, HDZJF reduced inflammation, promoted mucosal healing, improved body weight, and modulated protein expression related to EGFR/PI3K/AKT.DiscussionThe findings highlight HDZJF's capacity to alleviate RIOM by targeting the EGFR/PI3K/AKT pathway, thereby suppressing inflammatory responses and apoptotic processes. These results underscore HDZJF's translational potential for RIOM treatment and justify further clinical investigation into its therapeutic utility.

Investigating the PI3K/AKT/mTOR axis in Buzhong Yiqi Decoction’s anti-colorectal cancer activity

Buzhong Yiqi Decoction (BZYQD) is a traditional Chinese medicine renowned for its anti-colorectal cancer (CRC) properties. However, the bioactive components and mechanisms of BZYQD against CRC remain unknown. In this study, LC-MS was used to analyze the chemical composition of BZYQD. Next, the network pharmacology and molecular docking was used to investigate the core components and targets of BZYQD against CRC. Finally, we experimentally validated the potential mechanism of BZYQD against CRC through in vitro studies. Our results identified 26 chemical components in the BZYQD; 75 “hithubs” targets were screened by network pharmacology, and mainly involving pathways such as including pathways in cancer, P13K-Akt signaling pathway, proteoglycans in cancer, kaposi sarcoma-associated herpesvirus, and lipid and atherosclerosis signaling pathways. Based on the number of “hithubs” targets in the key pathways, the two most critical targets including AKT1 and PIK3CA were selected. The component-target network results indicated that astragaloside IV, gancaonin A, quercetin, poricoic acid A, and licoisoflavanone are key anti-CRC components in BZYQD. Molecular docking showed a strong binding affinity between these components and targets. The phosphoinositide 3-kinase (PI3K)/protein kinase B (AKT) signaling pathway emerged as the primary target of BZYQD. Further in vitro studies confirmed that BZYQD’s anti-CRC activity is mediated through the PI3K/AKT/mTOR axis and influences macrophage polarization. BZYQD exerts its therapeutic effects on CRC through multiple components, targets, and pathways. Our study elucidates the effective components and molecular mechanisms of BZYQD in CRC treatment and provides preliminary validation through molecular docking and experimental studies.

Raspberry ameliorates renal fibrosis in rats with chronic kidney disease via the PI3K/Akt pathway.

Raspberry ameliorates renal fibrosis in rats with chronic kidney disease via the PI3K/Akt pathway.

Yi-qi-yang-yin decoction ameliorates diabetic retinopathy: New and comprehensive evidence from network pharmacology, machine learning, molecular docking and molecular biology experiment.

Yi-qi-yang-yin decoction ameliorates diabetic retinopathy: New and comprehensive evidence from network pharmacology, machine learning, molecular docking and molecular biology experiment.

Network pharmacology combining molecular docking to unveil the anti-inflammatory mechanism of Aconitum Heterophyllum

ObjectiveThe objective of this study was to examine the impact and underlying mechanisms of Aconitum Heterophyllum in mitigating cellular inflammation.MethodsInitially, the principal components of A.heterophyllum were obtained from relevant literature sources, and the corresponding protein targets of A.heterophyllum were searched on Pubchem and Swiss Target Prediction database. Subsequently, the genes linked with inflammation were gathered from PHARMGKB, OMIM, and GeneCards databases. The core targets were screened, and a protein–protein interaction (PPI) network was constructed using Cytoscape 3.9.1. For general targets, the gene ontology (GO) analysis and Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis were conducted. Molecular docking was further applied for the core targets and compounds. Finally, the RAW264.7 cellular inflammation model was constructed, and MTT assay, Griess assay and qRT-PCR assay were used to initially validate the anti-inflammatory effects of A. heterophyllum and its underlying mechanisms.ResultsIn total, 35 compounds and 1322 targets were associated with A.heterophyllum, along with 3534 genes implicated in inflammation. The intersection analysis yielded 244 common targets, contributing to the enrichment of 146 pathways. Notably, results of molecular docking revealed strong binding between the active compounds and core targets. Furthermore, in vitro experiments indicated the anti-inflammatory potential of A.heterophyllum’s active ingredient through the modulation of the EGFR/JAK2/STAT3 pathway and EGFR-AKT pathway, as well as inhibiting cellular NO release to reduce the inflammatory response.ConclusionA.heterophyllum exerts anti-inflammatory activity by inhibiting EGFR-AKT1 activity and inhibiting EGFR/JAK2/STAT3 signal transduction.

Study on the Material Basis and Mechanisms of Achyrocline satureioides in the Treatment of Nonsmall Cell Lung Cancer Based on Network Pharmacology and Spatial Metabolomics.

Achyrocline satureioides have good therapeutic effects on nonsmall cell lung cancer (NSCLC). Nevertheless, it is still challenging to elucidate the active ingredients and mechanism of action due to their complex chemical composition. To address this, we innovatively combined network pharmacology with spatial metabolomics to comprehensively investigate the active components and the action mechanism in the present study. First, metabolomics of cells treated with the methanol extract of A. satureioides (ASM) utilizing high-resolution ultrahigh-performance liquid chromatography tandem mass spectrometry (HR-UHPLC-MS/MS) revealed 32 changed metabolites and 7 enriched metabolic pathways, confirming the anti-NSCLC effect of ASM and its impact on endogenous metabolites at the cellular level. Then, 69 chemical components in the ASM were identified using HR-UHPLC-MS/MS, followed by the screening of 6 core components and 10 core targets of anti-NSCLC with the help of network pharmacology and molecular docking. Lastly, quercetin, the most abundant compound among the six core active ingredients, was chosen for evaluating its anti-NSCLC effect and the potential mechanism using matrix-assisted laser desorption/ionization mass spectrometry imaging (MALDI-MSI). 51 altered endogenous metabolites were screened, and pathway enrichment analysis results were consistent with cell metabolomics, corroborating our network pharmacology predictions. In addition, we also observed the accumulation of three metabolites of quercetin in the tumor tissues. Network pharmacology combined with MSI elucidated the metabolic mechanisms by which A. satureioides treats NSCLC, offering new insights into herbal cancer therapies.

QingReDu capsule ameliorates psoriasis vulgaris by regulating EZH2/NF-κB signaling pathway.

QingReDu Capsule is commonly used clinically to treat psoriasis vulgaris, the mechanism of treating psoriasis vulgaris is still unclear. Using the ultra-performance liquid chromatography-quadrupole time-of-flight mass spectrometry (UPLC-Q-TOF-MS/MS), we analyzed the components in rat plasma after QingReDu Capsule administration. We then predicted the mechanistic pathways of QingReDu Capsule in ameliorating psoriasis vulgaris by screening the intersecting targets of the QingReDu Capsule plasma entry components and psoriasis vulgaris using network pharmacology and molecular docking. Combined with pharmacodynamic evaluation and HE staining, we investigated the efficacy and mechanism of QingReDu Capsule in treating psoriasis vulgaris. Forty-one compounds were identified in the rat plasma after QingReDu Capsule administration, thirty-seven QingReDu Capsule components with the InChI SMILES structure were screened, and two hundred and thirty-five targets intersected with psoriasis vulgaris. network pharmacology revealed that QingReDu Capsule is not only involved in the regulation of the inflammatory response, reactive oxygen species metabolism, and intracellular oxidative stress, but also related to the nuclear factor kappa-B (NF-κB) and mitogen-activated protein kinase (MAPK) signaling pathways. The molecular docking results showed that 10 components, including Myristicin, had good affinity with the screened core targets. The pharmacodynamic results showed that QingReDu Capsule reduced the serum levels of tumor necrosis factor α (TNF-α), interleukin 17 (IL-17), and interleukin 23 (IL-23) by down-regulating the protein levels of enhancer of Zeste Homolog 2 (EZH2) and NF-κB, reduced erythema and the scaling of skin lesions, and treated histopathological damage to the skin, such as hyperkeratosis with keratosis imperfecta and the thickening of the sphenoid layer. These findings illustrated that QingReDu Capsule treat psoriasis vulgaris by affecting the EZH2/NF-κB signaling pathway and influencing the level of inflammatory factors.

Network Pharmacological Analysis of Hydroxychloroquine Intervention in the Treatment of Iga Nephropathy.

IgA nephropathy (IgAN) is the most prevalent primary glomerulonephritis globally and has a high propensity to develop into end-stage renal disease (ESRD). Hydroxychloroquine has been proven to reduce proteinuria in IgAN patients, but the precise mechanism remains unclear. Therefore, network pharmacology was used to investigate the mechanism. PubChem and SwissADME databases were utilized to acquire the structure of hydroxychloroquine. The SwissTargetPrediction, PharmMapper, DrugBank, TargetNet, and BATMAN-TCM databases were then utilized to obtain the targets. The target genes related to IgAN were then gathered from the databases, which included GeneCards, PHARMGKB, DrugBank, OMIM, and DisGeNET. Common targets were obtained by UniProt. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses were performed to define the main molecular mechanisms and pathways. Furthermore, a protein-protein interaction (PPI) network was constructed using the STRING tool, and the core targets were obtained by Cytoscape. Finally, molecular docking between the core targets and hydroxychloroquine was performed. 167 common target genes were acquired by overlapping. The core targets were TNF, ALB, IL1B, JUN, FOS, SRC, and MMP9. The GO and KEGG results showed the targets to be related to the production of inflammatory cytokines and chemokines and were engaged in the toll-like receptor (TLR) signaling pathway. At the same time, the molecular docking results showed that the core targets all combined with hydroxychloroquine closely. This study proved that hydroxychloroquine may treat IgAN through the TLR signaling pathway, and the restraint of TNF, TLR, IL1B, and JUN may be essential for the treatment.

The Jieduquyuziyin prescription alleviates systemic lupus erythematosus by modulating B cell metabolic reprogramming via the AMPK/PKM2 signaling pathway.

The Jieduquyuziyin prescription alleviates systemic lupus erythematosus by modulating B cell metabolic reprogramming via the AMPK/PKM2 signaling pathway.

Network Pharmacology, Molecular Docking, and Experimental Validation on Guiluoshi Anzang Decoction Against Premature Ovarian Insufficiency.

Premature Ovarian Insufficiency (POI) is a disease suffered by women under the age of 40 when ovarian function has declined, seriously affecting both the physical and mental health of women. Guiluoshi Anzang decoction (GLSAZD) has been used for a long time and has a unique therapeutic effect on improving ovarian function. This study aims to investigate the mechanism of GLSAZD in treating POI through network pharmacology, molecular docking, and experimental verification. In this study, the active ingredients of Guiluoshi Anzang Decoction and the targets of POI were obtained from TCMSP, BATMANN-TCM, Uniprot, GeneCards, and other databases, and network pharmacology analysis was performed. Molecular docking was conducted to validate the affinity of the main active ingredient of GLSAZD to key POI targets. A POI SD rat model was established, and HE staining, ELISA, Real-time PCR, and Western blot experiments were performed to verify the predicted core targets and the therapeutic effects. 10 core targets and the top 5 ingredients were screened out. Molecular docking showed core targets AKT1, CASP3, TNF, TP53, and IL6 had stable binding with the core 5 ingredients quercetin, kaempferol, beta-sitosterol, luteolin, and Stigmasterol. GO and KEGG enrichment analysis demonstrated the mechanism involved in the positive regulation of gene expression, PI3K-AKT signaling pathway, and apoptosis signaling pathways. Animal experiments indicated GLSAZD could up-regulate the protein expression of p-PI3K and p-AKT1 and the mRNA expression of STAT3 and VEGF, down-regulate TP53 and Cleaved Caspase-3 protein expression in rat`s ovarian tissues and serum TNF-α and IL-6 protein levels, activate PI3K-AKT signaling pathway and inhibit the apoptosis signaling pathway. GLSAZD treats POI through multi-component, multi-target, and multi-pathway approaches. This study provided evidence for its clinical application in treating POI and shed light on the study of traditional medicine of the Guangxi Zhuang Autonomous Region in China.