Xiaotan Sanjie decoction attenuates tumor angiogenesis by manipulating Notch-1-regulated proliferation of gastric cancer stem-like cells

AIM: To determine the underlying mechanisms of action and influence of Xiaotan Sanjie (XTSJ) decoction on gastric cancer stem-like cells (GCSCs).

Yangzheng Sanjie decoction regulates proliferation and apoptosis of gastric cancer cells by enhancing let-7a expression

AIM To explore the let-7a-mediated anti-cancer effect of Yangzheng Sanjie decoction(YZSJD) in gastric cancer(GC) cells.METHODS YZSJD-containing serum(YCS) was prepared using traditional Chinese medicine serum pharmacology methods. After YCS treatment, cell proliferation and apoptosis were assessed by cell counting kit-8 assay and flow cytometry, respectively, and mi RNA expression profiles were determined using q PCR arrays. Let-7a expression was examined by in situ hybridization in GC tissues and by q PCR in GC cells. c-Myc protein expression was detected by immunohistochemistry in GC tissues, and by Western blot in cell lines.RESULTS YZSJD significantly inhibited proliferation and induced apoptosis in AGS and HS-746 T GC cells. After treatment with YCS, the mi RNA expression profiles were altered and the reduced let-7a levels in both cell lines were up-regulated, accompanied by a decrease in c-Myc expression. Moreover, decreased let-7a expression and increased c-Myc expression were observed during the progression of gastric mucosa cancerization.CONCLUSION YZSJD inhibits proliferation and induces apoptosis of GC cells by restoring the aberrant expression of let-7a and c-Myc.

Mechanism underlying efficacy of Shugan Sanjie decoction(疏肝散结汤) on plasma cell mastitis,based on network pharmacology and experimental verification

OBJECTIVE:To investigate the mechanism underpinning the effeicay of Shugan Sanjie decoction(疏肝散结汤,SGSJD)on plasma cell mastitis(PCM)based on network pharmacology,and to verify it through in vitro.METHODS:Traditional Chinese Medicine Systems Pharmacology Database and Analysis Platform and Bioinformatics Analysis Tool for Molecular mechanism of Traditional Chinese Medicine were used to screen effective compounds and drug targets;Online Mendelian Inheritance in Man and Gene Cards were used to search for PCM targets.The potential targets of SGSJD in treating PCM were obtained after the drug targets and disease targets were crossed.Cytoscape software was used to establish and analyze the network of Chinese medicines-active compounds-targets-disease;STRING database platform was used to analyze Protein Protein Interaction network;Bioconductor software package was used to perform Gene ontology and Kyoto Encyclopedia of Genes and Genomes enrichment for potential targets.Western blot analysis was used to verify the janus kinase/signal transducer and activator of transcription(JAK-STAT)pathway in vitro.RESULTS:(a)47 potential pharmacological components of SGSJD treatment of PCM were screened including quercetin,luteolin,kaempferol and others;20 common targets were obtained,including interleukin-6(IL-6),epidermal growth factor receptor,estrogen receptor 1,nitric oxide synthase 3 and others;a number of signal pathways were available,of which advanced glycation end product/receptor for advanced glycation end products signaling pathway in diabetic complications,hypoxia-inducible factor 1 signaling pathway and janus tyrosine kinase-signal transducer and transcription activator(JAK-STAT)signaling pathway were the main signal pathways related to PCM.(b)Compared with the Blank group,the expressions of p-JAK2/JAK2,pSTAT3/STAT3 and IL-6 protein in the Model group were significantly increased(P<0.01);Compared with the Model group,the expression of p-JAK2/JAK2,p-STAT3/STAT3,and IL-6 protein in the treatment group were significantly reduced in a dose-dependent manner(P<0.05).Compared with the Model group,the dexamethasone significantly reduced the expression of p-JAK2/JAK2,p-STAT3/STAT3,and IL-6(P<0.01).CONCLUSIONS:The SGSJD may regulate the JAKSTAT signaling pathway to achieve the effect of treating PCM by reducing the expression of p-JAK2/JAK2,p-STAT3/STAT3 and IL-6 in a dose-dependent manner.