<i>Scutellaria baicalensis</i> in the Treatment of Hepatocellular Carcinoma: Network Pharmacology Analysis and Experimental Validation

Cai, Xin; Shi, Peng; Wang, Li; Tang, Dongling; Zhang, Pingan

doi:10.1155/2023/4572660

Cited by 5 publications

(1 citation statement)

References 27 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The major risk factor for HCC is chronic infection with hepatitis B virus or hepatitis C virus, which account for 56% and 20% of HCC deaths globally, respectively (Granata et al., 2021). In addition, smoking, alcoholism, non‐alcoholic fatty liver disease, obesity, and aflatoxin exposure may also lead to HCC (Cai et al., 2023). Even though surgical operations, interventional therapy, chemoradiotherapy and liver transplantation improve the prognosis of the patients, HCC recurrence rate and mortality are still high due to the high aggressiveness and treatment resistance (Chen et al., 2021; Chen et al., 2022).…”

Section: Introductionmentioning

confidence: 99%

Exploring the mechanism of bioactive components of Prunella vulgaris L. in treating hepatocellular carcinoma based on network pharmacology

Tu,

Feng,

Wang

et al. 2023

Chem Biol Drug Des

View full text Add to dashboard Cite

In traditional Chinese Medicine, Prunella vulgaris L. (PVL) is potentially effective in the treatment of some human malignancies including hepatocellular carcinoma (HCC). However, the detailed mechanism of action remains unclear. The purpose of this study was to decipher the constitutes of the bioactive ingredients of PVL, and its mechanism against HCC using network pharmacology and in vitro experiments. The bioactive components of PVL were obtained by Traditional Chinese Medicine System Pharmacology Database and Analysis platform database, and the targets of bioactive components of PVL was investigated by Swiss Target Prediction database. HCC related targets were obtained from GEO database, GeneCards database and DisGeNET database, and the gene ontology function annotation and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis were conducted for annotating the biological function of gene targets. A protein–protein interaction network was constructed using STRING database. Molecular docking of key bioactive ingredients was performed using AutoDock Vina. Cell proliferation and apoptosis were detected by cell counting kit‐8 and flow cytometry, respectively. The expression level of the target genes of PI3K/Akt pathway were detected by qPCR. In the present work, 11 bioactive components of PVL were screened out, which acted on 177 potential targets. In addition, 13,517 genes were strongly associated with HCC pathogenesis, of which 158 targets are overlapped with PVL's targets. KEGG results identified 39 signaling pathways closely associated with the 158 targets. Molecular docking showed that the main bioactive components of PVL, kaempferol, morin, quercetin, luteolin, and spinasterol, had good binding activity with the core proteins in cancer biology such as AKT1, EGFR, SRC, ESR1, and PPARG. In vitro assays showed that quercetin, one of the main components of PVL extracts effectively inhibited HCC cell proliferation, and promoted apoptosis, which may be associated with PI3K/AKT signaling pathway. In summary, PVL may regulate HCC progression by regulating core targets such as AKT1, EGFR, SRC, ESR1, and PPARG, and acting on PI3K‐Akt signaling pathway.

show abstract

Section: Introductionmentioning

confidence: 99%

Exploring the mechanism of bioactive components of Prunella vulgaris L. in treating hepatocellular carcinoma based on network pharmacology

Tu,

Feng,

Wang

et al. 2023

Chem Biol Drug Des

View full text Add to dashboard Cite

show abstract

Baicalein, a natural flavonoid in gastrointestinal cancers treatment: recent trends and future perspectives

Sharma,

Pal,

Gill

et al. 2024

Med Oncol

View full text Add to dashboard Cite

Hua-Feng-Dan Alleviates LPS-induced Neuroinflammation by Inhibiting the TLR4/Myd88/NF-κB Pathway: Integrating Network Pharmacology and Experimental Validation

Zhang,

Pei,

Zheng

et al. 2024

CPD

View full text Add to dashboard Cite

aims: Our study aims to elucidate the molecular mechanism by which HFD mitigates neuroinflammation through combining network pharmacology and experimental validation. background: Neuroinflammation is the pathological basis of many neurological diseases, including neurodegenerative diseases and stroke. Hua-Feng-Dan (HFD) is a well-established traditional Chinese medicine used for the treatment of stroke and various other brain-related ailments. objective: Our study aims to elucidate the molecular mechanism by which HFD mitigates neuroinflammation through combining network pharmacology and experimental validation. method: Active compounds and their related targets were extracted from the TCMSP database and SymMap database. The neuroinflammation-related targets were obtained from the GeneCards database. Protein-protein interaction (PPI) network was constructed using the common target of HFD and neuroinflammation. MCODE plug-in was used to find the hub module genes. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analyses were employed to dissect the hub module genes. The lipopolysaccharide (LPS)-induced BV2 microglial neuroinflammation model was utilized to assess the therapeutic effects of HFD on neuroinflammation. Western blotting analysis was performed to examine the core target proteins in the TLR4/MyD88/NF-κB signaling pathway, potentially implicated in HFD's therapeutic effects on neuroinflammation. Hoechest 33342 staining and JC-1 staining were employed to evaluate the effect of inflammatory factors secreted by activated microglia on neuronal apoptosis. result: Through network pharmacology, 73 active compounds were identified, with quercetin, beta-sitosterol, luteolin, and (-)-Epigallocatechin-3-Gallate recognized as important compounds. Meanwhile, 115 common targets of HFD and neuroinflammation were identified and 61 targets were selected as the hub targets utilizing the MCODE algorithm. The results of in vitro experiments demonstrated that HFD significantly inhibited microglial-mediated neuronal inflammation induced by LPS. Integrating the predictions from network pharmacology with the results of in vitro experiments, we discerned that the mechanism of HFD in mitigating neuroinflammation is closely related to TLR4/MyD88/NF-κB pathway. Furthermore, HFD demonstrates a capacity to shield neurons from apoptosis by curbing the secretion of pro-inflammatory factors subsequent to microglial activation. conclusion: Our findings demonstrated that HFD had an inhibitory effect on LPS-induced neuroinflammation in microglia and elucidated its underlying mechanism. These findings will provide theoretical underpinning for using HFD in clinical treatment of neurodegenerative diseases related to neuroinflammation. other: No

show abstract

Scutellaria baicalensis in the Treatment of Hepatocellular Carcinoma: Network Pharmacology Analysis and Experimental Validation

Cited by 5 publications

References 27 publications

Exploring the mechanism of bioactive components of Prunella vulgaris L. in treating hepatocellular carcinoma based on network pharmacology

Exploring the mechanism of bioactive components of Prunella vulgaris L. in treating hepatocellular carcinoma based on network pharmacology

Baicalein, a natural flavonoid in gastrointestinal cancers treatment: recent trends and future perspectives

Hua-Feng-Dan Alleviates LPS-induced Neuroinflammation by Inhibiting the TLR4/Myd88/NF-κB Pathway: Integrating Network Pharmacology and Experimental Validation

Contact Info

Product

Resources

About