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Article ; Online: Xijiao Dihuang decoction combined with Yinqiao powder promotes autophagy-dependent ROS decrease to inhibit ROS/NLRP3/pyroptosis regulation axis in influenza virus infection.

Deng, Di / Zhao, Mengfan / Liu, Huanwei / Zhou, Siyao / Liu, Hui / You, Leiming / Hao, Yu

Phytomedicine : international journal of phytotherapy and phytopharmacology

2024 Volume 128, Page(s) 155446

Abstract: Background: Influenza viral pneumonia is a common complication after influenza virus infection. Xijiao Dihuang Decoction combined with Yinqiao Powder (XDY) is effective on improving influenza viral pneumonia.: Purpose: This study further explores the ...

Abstract	Background: Influenza viral pneumonia is a common complication after influenza virus infection. Xijiao Dihuang Decoction combined with Yinqiao Powder (XDY) is effective on improving influenza viral pneumonia. Purpose: This study further explores the anti-inflammatory mechanism of XDY in the treatment of influenza viral pneumonia. Study design: The effects of XDY on inflammation, autophagy, NACHT-LRR-PYD-containing protein 3 (NLRP3) inflammasome and pyroptosis were assessed in the mice with influenza viral pneumonia. In addition, the mouse macrophage cell line (J774A.1) infected with influenza virus was adopted to decode the in vitro effects of XDY on autophagy, reactive oxygen species (ROS), NLRP3 inflammasome and pyroptosis. We analyzed the XDY-induced autophagy, especially the mitophagy-related ROS clearance, and the subsequent inhibition of ROS/NLRP3 inflammasome/pyroptosis signaling in the infected macrophages by different assays based on quantitative polymerase chain reaction, western blot, flow cytometry, immunofluorescence and enzyme-linked immunosorbent assay. Results: In vivo, XDY could effectively improve the lung inflammatory response in the mice with influenza virus pneumonia, due to an intact autophagy flux-promoting effect and the inhibiting roles on NLRP3 inflammasome and pyroptosis. Notably, in vitro, compared with the infected macrophages treated by the NLRP3 inflammasome agonist (Monosodium urate) or the mitochondrial-targeted antioxidant agent, the XDY-dependent treating could inhibit pyroptosis by negatively regulating the signaling axis of ROS/NLRP3 inflammasome/pyroptosis in the influenza virus-infected macrophages. More interestingly, XDY could promote an intact autophagy flux, inducing mitophagy eliminating the damaged mitochondria to reduce the intracellular ROS accumulation, and thus decrease the oxidative stress in the infected macrophages. Especially, the inhibitor of autophagy inition, 3-Methyladenine, could reverse the inhibitory effect of XDY on ROS-NLRP3 inflammasome-mediated pyroptosis, indicating an XDY-promoted mitophagy-dependent ROS scavenging. Conclusion: XDY can promote an intact autophagy flux to eliminate damaged mitochondria, namely mitophagy, which reduces the intracellular ROS accumulation contributing to NLRP3 inflammasome activation, restricting pyroptosis and eventually alleviating the influenza virus-induced inflammatory lesions. The obtained results provide new insights into the mechanism of action of XDY in alleviating influenza virus pneumonia, especially the roles of XDY in anti-oxidation, anti-inflammation and anti-pyroptosis, with potential therapeutic targets for future application in integrative medicine.
MeSH term(s)	Animals ; Drugs, Chinese Herbal/pharmacology ; NLR Family, Pyrin Domain-Containing 3 Protein/metabolism ; Pyroptosis/drug effects ; Reactive Oxygen Species/metabolism ; Mice ; Autophagy/drug effects ; Orthomyxoviridae Infections/drug therapy ; Inflammasomes/metabolism ; Inflammasomes/drug effects ; Macrophages/drug effects ; Macrophages/metabolism ; Cell Line ; Mice, Inbred C57BL ; Male ; Lung/drug effects ; Lung/virology
Chemical Substances	Drugs, Chinese Herbal ; NLR Family, Pyrin Domain-Containing 3 Protein ; Reactive Oxygen Species ; Nlrp3 protein, mouse ; yinqiao ; Inflammasomes
Language	English
Publishing date	2024-02-10
Publishing country	Germany
Document type	Journal Article
ZDB-ID	1205240-1
ISSN	1618-095X ; 0944-7113
ISSN (online)	1618-095X
ISSN	0944-7113
DOI	10.1016/j.phymed.2024.155446
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Article ; Online: Berberine ameliorates pulmonary inflammation in mice with influenza viral pneumonia by inhibiting NLRP3 inflammasome activation and gasdermin D-mediated pyroptosis.

An, Chen / Wu, Yanmin / Wu, Jun / Liu, Huanwei / Zhou, Siyao / Ge, Dongyu / Dong, Ruijuan / You, Leiming / Hao, Yu

Drug development research

2022 Volume 83, Issue 7, Page(s) 1707–1721

Abstract: Viral pneumonia is a common complication caused by Influenza A virus infection and is characterized by severe pulmonary inflammation. A previous study showed that berberine (BBR) significantly ameliorated the pulmonary inflammation in mice with influenza ...

Abstract	Viral pneumonia is a common complication caused by Influenza A virus infection and is characterized by severe pulmonary inflammation. A previous study showed that berberine (BBR) significantly ameliorated the pulmonary inflammation in mice with influenza viral pneumonia but its underlying mechanism is not entirely understood. In this study, we reproduced the mouse model of influenza viral pneumonia through intranasal infection of A/Puerto Rico/8/34 (H1N1), to further investigate the anti-inflammatory mechanism of BBR based on nucleotide-binding oligomerization domain-like receptor protein (NLRP) 3 inflammasome activation and Gasdermin D (GSDMD)-mediated pyroptosis. Consistent with MCC950 (10 mg/kg, a specific NLRP3 inflammasome inhibitor), BBR (10 mg/kg) obviously improved the weight loss and survival rate of infected mice, alleviated their pulmonary inflammation, and suppressed the accumulation of tumor necrosis factor and interleukin (IL)-6 in lungs without obvious inhibition on viral multiplication (hemagglutinin titer and nucleoprotein messenger RNA). Moreover, BBR (10 mg/kg) reduced the expressions of NLRP3, apoptosis-associated speck-like protein containing a CARD (ASC), and cysteinyl aspartate-specific proteinase (Caspase)1 (Caspase1 precursor [Pro-caspase1] + Caspase1p20 subunit) and the ratio of Caspase1p20 subunit to Caspase1, thus inhibiting the NLRP3 inflammasome activation and resulting in the decreased contents of mature IL-1β and IL-18 in lungs. The GSDMD expression (GSDMD precursor [Pro-GSDMD] + GSDMD-N terminal [NT]) and the ratio of GSDMD-NT to GSDMD were also declined by BBR (10 mg/kg). These evidence indicate that BBR may ameliorate pulmonary inflammation in mice with influenza viral pneumonia through inhibiting NLRP3 inflammasome activation, as well as depressing GSDMD-mediated pyroptosis via declining GSDMD expression and restraining NLRP3 inflammasome-mediated GSDMD activation.
MeSH term(s)	Animals ; Mice ; Berberine/pharmacology ; Inflammasomes/metabolism ; Influenza A Virus, H1N1 Subtype ; NLR Family, Pyrin Domain-Containing 3 Protein/metabolism ; Pneumonia, Viral/drug therapy ; Pyroptosis ; Orthomyxoviridae Infections/complications ; Orthomyxoviridae Infections/drug therapy
Chemical Substances	Berberine (0I8Y3P32UF) ; Inflammasomes ; NLR Family, Pyrin Domain-Containing 3 Protein ; Nlrp3 protein, mouse
Language	English
Publishing date	2022-09-16
Publishing country	United States
Document type	Journal Article
ZDB-ID	604587-x
ISSN	1098-2299 ; 0272-4391
ISSN (online)	1098-2299
ISSN	0272-4391
DOI	10.1002/ddr.21995
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Article ; Online: Identification of a disulfidptosis-related genes signature for prognostic implication in lung adenocarcinoma.

Huang, Jiaqi / Zhang, Jingyuan / Zhang, Fanqin / Lu, Shan / Guo, Siyu / Shi, Rui / Zhai, Yiyan / Gao, Yifei / Tao, Xiaoyu / Jin, Zhengsen / You, Leiming / Wu, Jiarui

Computers in biology and medicine

2023 Volume 165, Page(s) 107402

Abstract: Background: Lung adenocarcinoma (LUAD) is the most prevalent subtype of non-small cell lung cancer. Additionally, disulfidptosis, a newly discovered type of cell death, has been found to be closely associated with the onset and progression of tumors.: ...

Abstract	Background: Lung adenocarcinoma (LUAD) is the most prevalent subtype of non-small cell lung cancer. Additionally, disulfidptosis, a newly discovered type of cell death, has been found to be closely associated with the onset and progression of tumors. Methods: The study first identified genes related to disulfidptosis through correlation analysis. These genes were then screened using univariate cox regression and LASSO regression, and a prognostic model was constructed through multivariate cox regression. A nomogram was also created to predict the prognosis of LUAD. The model was validated in three independent data sets: GSE72094, GSE31210, and GSE37745. Next, patients were grouped based on their median risk score, and differentially expressed genes between the two groups were analyzed. Enrichment analysis, immune infiltration analysis, and drug sensitivity evaluation were also conducted. Results: In this study, we examined 21 genes related to disulfidptosis and developed a gene signature that was found to be associated with a poorer prognosis in LUAD. Our model was validated using three independent datasets and showed AUC values greater than 0.5 at 1, 3, and 5 years. Enrichment analysis revealed that the disulfidptosis-related genes signature had a multifaceted impact on LUAD, particularly in relation to tumor development, proliferation, and metastasis. Patients in the high-risk group exhibited higher tumor purity and lower stromal score, ESTIMATE score, and Immune score. Conclusion: This study constructed a gene signature related to disulfidptosis in lung adenocarcinoma and analyzed its impact on the disease and its association with the tumor microenvironment. The findings of this research provide valuable insights into the understanding of lung adenocarcinoma and could potentially lead to the development of new treatment strategies.
MeSH term(s)	Humans ; Prognosis ; Carcinoma, Non-Small-Cell Lung ; Lung Neoplasms/genetics ; Adenocarcinoma of Lung/genetics ; Tumor Microenvironment
Language	English
Publishing date	2023-08-28
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	127557-4
ISSN	1879-0534 ; 0010-4825
ISSN (online)	1879-0534
ISSN	0010-4825
DOI	10.1016/j.compbiomed.2023.107402
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Zs.A 653: Show issues

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Article ; Online: Identification of an immune-related 6-lncRNA panel with a good performance for prognostic prediction in hepatocellular carcinoma by integrated bioinformatics analysis.

Lu, Shan / Liu, Xinkui / Wu, Chao / Zhang, Jingyuan / Stalin, Antony / Huang, Zhihong / Tan, Yingying / Wu, Zhishan / You, Leiming / Ye, Peizhi / Fu, Changgeng / Zhang, Xiaomeng / Wu, Jiarui

Medicine

2023 Volume 102, Issue 29, Page(s) e33990

Abstract: Hepatocellular carcinoma (HCC) is one of the most malignant tumors with a poor prognosis. The long non-coding RNA (lncRNA) has been found to have great potential as a prognostic biomarker or therapeutic target for cancer patients. However, the prognostic ...

Abstract	Hepatocellular carcinoma (HCC) is one of the most malignant tumors with a poor prognosis. The long non-coding RNA (lncRNA) has been found to have great potential as a prognostic biomarker or therapeutic target for cancer patients. However, the prognostic value and tumor immune infiltration of lncRNAs in HCC has yet to be fully elucidated. To identify prognostic biomarkers of lncRNA in HCC by integrated bioinformatics analysis and explore their functions and relationship with tumor immune infiltration. The prognostic risk assessment model for HCC was constructed by comprehensively using univariate/multivariate Cox regression analysis, Kaplan-Meier survival analysis, and the least absolute shrinkage and selection operator regression analysis. Subsequently, the accuracy, independence, and sensitivity of our model were evaluated, and a nomogram for individual prediction in the clinic was constructed. Tumor immune microenvironment (TIME), immune checkpoints, and human leukocyte antigen alleles were compared in high- and low-risk patients. Finally, the functions of our lncRNA signature were examined using Gene Ontology, Kyoto Encyclopedia of Genes and Genomes enrichment analysis, and gene set enrichment analysis. A 6-lncRNA panel of HCC consisting of RHPN1-AS1, LINC01224, CTD-2510F5.4, RP1-228H13.5, LINC01011, and RP11-324I22.4 was eventually identified, and show good performance in predicting the survivals of patients with HCC and distinguishing the immunomodulation of TIME of high- and low-risk patients. Functional analysis also suggested that this 6-lncRNA panel may play an essential role in promoting tumor progression and immune regulation of TIME. In this study, 6 potential lncRNAs were identified as the prognostic biomarkers in HCC, and the regulatory mechanisms involved in HCC were initially explored.
MeSH term(s)	Humans ; Carcinoma, Hepatocellular/genetics ; RNA, Long Noncoding/genetics ; Prognosis ; Liver Neoplasms/genetics ; Computational Biology ; Biomarkers ; Biomarkers, Tumor/genetics ; Tumor Microenvironment/genetics
Chemical Substances	RNA, Long Noncoding ; Biomarkers ; Biomarkers, Tumor
Language	English
Publishing date	2023-07-21
Publishing country	United States
Document type	Journal Article
ZDB-ID	80184-7
ISSN	1536-5964 ; 0025-7974
ISSN (online)	1536-5964
ISSN	0025-7974
DOI	10.1097/MD.0000000000033990
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Article ; Online: Compound Kushen Injection inhibits epithelial-mesenchymal transition of gastric carcinoma by regulating VCAM1 induced by the TNF signaling pathway.

Huang, Zhihong / Wu, Chao / Zhou, Wei / Lu, Shan / Tan, Yingying / Wu, Zhishan / You, Rongli / Stalin, Antony / Guo, Fengying / Zhang, Jingyuan / Liu, Pengyun / Wang, Wei / Duan, Xiaoxia / You, Leiming / Wu, Jiarui

Phytomedicine : international journal of phytotherapy and phytopharmacology

2023 Volume 118, Page(s) 154984

Abstract: Background: Gastric carcinoma (GC) treatment needs to be developed rapidly. Compound Kushen Injection (CKI), a formula from traditional Chinese medicine, has been used clinically in combination with chemotherapy to treat GC with satisfactory results. ... ...

Abstract	Background: Gastric carcinoma (GC) treatment needs to be developed rapidly. Compound Kushen Injection (CKI), a formula from traditional Chinese medicine, has been used clinically in combination with chemotherapy to treat GC with satisfactory results. However, the molecular mechanism by which CKI acts to cure GC is still unclear. Methods: In the present study, in vivo and in vitro experiments were used to assess the efficacy of CKI. Using ceRNA microarray and TMT technologies, the molecular mechanism of CKI was further investigated at the transcriptional and protein levels, and a bioinformatics approach was employed to investigate and functionally validate key CKI targets in GC. Results: When combined with cisplatin (DDP), CKI significantly increased its efficacy in preventing the proliferation and metastasis of GC cells and malignant-looking tumors in mice. High-throughput sequencing data and bioinformatics analysis showed that CKI regulated the TNF signaling pathway, epithelial-mesenchymal transition (EMT), with VCAM1 as a key target. The transcription factors CEBPB, JUN, RELA, NFKB1, the EMT mesenchymal-like cell markers N-cadherin and vimentin, as well as the expression of VCAM1 and its upstream signaling driver TNF, were all downregulated by CKI. In contrast, the expression of the EMT epithelial-like cell marker E-cadherin was upregulated. Conclusion: CKI can effectively inhibit GC growth and metastasis, improve body's immunity, and protect normal tissues from damage. The molecular mechanism by which CKI inhibits metastasis of GC is by regulating VCAM1 induced by the TNF signaling pathway to inhibit EMT of GC. Our results provide an important clue to clarify precisely the multi-scale molecular mechanism of CKI in the treatment of GC.
MeSH term(s)	Animals ; Mice ; Epithelial-Mesenchymal Transition ; Antineoplastic Agents/pharmacology ; Signal Transduction ; Stomach Neoplasms/genetics ; Cadherins ; Carcinoma ; Cell Line, Tumor
Chemical Substances	kushen (IYR6K8KQ5K) ; Antineoplastic Agents ; Cadherins
Language	English
Publishing date	2023-07-17
Publishing country	Germany
Document type	Journal Article
ZDB-ID	1205240-1
ISSN	1618-095X ; 0944-7113
ISSN (online)	1618-095X
ISSN	0944-7113
DOI	10.1016/j.phymed.2023.154984
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Article ; Online: Data mining combines bioinformatics discover immunoinfiltration-related gene SERPINE1 as a biomarker for diagnosis and prognosis of stomach adenocarcinoma.

Zhai, Yiyan / Liu, Xinkui / Huang, Zhihong / Zhang, Jingyuan / Stalin, Antony / Tan, Yingying / Zhang, Fanqin / Chen, Meilin / Shi, Rui / Huang, Jiaqi / Wu, Chao / Wu, Zhishan / Lu, Shan / You, Leiming / Wu, Jiarui

Scientific reports

2023 Volume 13, Issue 1, Page(s) 1373

Abstract: Stomach adenocarcinoma (STAD) is a type of cancer which often at itsadvanced stage apon diagnosis and mortality in clinical practice. Several factors influencethe prognosis of STAD, including the expression and regulation of immune cells in the tumor ... ...

Abstract	Stomach adenocarcinoma (STAD) is a type of cancer which often at itsadvanced stage apon diagnosis and mortality in clinical practice. Several factors influencethe prognosis of STAD, including the expression and regulation of immune cells in the tumor microenvironment. We here investigated the biomarkers related to the diagnosis and prognosis of gastric cancer, hoping to provide insights for the diagnosis and treatment of gastric cancer in the future. STAD and normal patient RNA sequencing data sets were accessed from the cancer genome atlas (TCGA database). Differential genes were determined and obtained by using the R package DESeq2. The stromal, immune, and ESTIMATE scores are calculated by the ESTIMATE algorithm, followed by the modular genes screening using the R package WGCNA. Subsequently, the intersection between the modular gene and the differential gene was taken and the STRING database was used for PPI network module analysis. The R packages clusterProfiler, enrichplot, and ggplot2 were used for GO and KEGG enrichment analysis. Cox regression analysis was used to screen survival-related genes, and finally, the R package Venn Diagram was used to take the intersection and obtain 7 hub genes. The time-dependent ROC curve and Kaplan-Meier survival curve were used to find the SERPINE1 gene, which plays a critical role in prognosis. Finally, the expression pattern, clinical characteristics, and regulatory mechanism of SERPINE1 were analyzed in STAD. We revealed that the expression of SERPINE1 was significantly increased in the samples from STAD compared with normal samples. Cox regression, time-dependent ROC, and Kaplan-Meier survival analyses demonstrated that SERPINE1 was significantly related to the adverse prognosis of STAD patients. The expression of SERPINE1 increased with the progression of T, N, and M classification of the tumor. In addition, the results of immune infiltration analysis indicated that the immune cells' expression were higher in high SERPINE1 expression group than that in low SERPINE1 expression group, including CD4
MeSH term(s)	Humans ; Stomach Neoplasms/diagnosis ; Stomach Neoplasms/genetics ; CD8-Positive T-Lymphocytes ; Prognosis ; Biomarkers ; Adenocarcinoma/diagnosis ; Adenocarcinoma/genetics ; Computational Biology ; Data Mining ; Tumor Microenvironment/genetics ; Plasminogen Activator Inhibitor 1/genetics
Chemical Substances	Biomarkers ; SERPINE1 protein, human ; Plasminogen Activator Inhibitor 1
Language	English
Publishing date	2023-01-25
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2615211-3
ISSN	2045-2322 ; 2045-2322
ISSN (online)	2045-2322
ISSN	2045-2322
DOI	10.1038/s41598-023-28234-7
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Elucidating the pharmacological effects of Compound Kushen injection on MYC-P15-CCND1 signaling pathway in nasopharyngeal carcinoma - An in vitro study.

Wu, Zhishan / Wu, Chao / Shi, Jian / Huang, Zhihong / Lu, Shan / Tan, Yingying / You, Rongli / Hai, Lina / Huang, Jiaqi / Guo, Siyu / Gao, Yifei / Jin, Zhengsen / Tao, Xiaoyu / You, Leiming / Wu, Jiarui

Journal of ethnopharmacology

2023 Volume 315, Page(s) 116702

Abstract: Ethnopharmacological relevance: Compound Kushen injection (CKI) is a representative medication of Chinese herbal injection and is often used in the adjuvant treatment of nasopharyngeal carcinoma (NPC), but its antitumor mechanism is poorly understood.!## ...

Abstract	Ethnopharmacological relevance: Compound Kushen injection (CKI) is a representative medication of Chinese herbal injection and is often used in the adjuvant treatment of nasopharyngeal carcinoma (NPC), but its antitumor mechanism is poorly understood. Aim of the study: To preliminarily elucidate the effects and possible mechanisms of CKI on NPC. Methods: In this work, we explored the possible molecular mechanisms of CKI against NPC by using network pharmacology and molecular docking. In addition, proteomics was used to explore the localization and quantitative information of protein in NPC C666-1 cells after the intervention of CKI, and enrichment analysis was used to obtain the potential targets and pathways. Finally, the effect and the core targets of CKI in the intervention of NPC were explored in vitro experiments. Results: Network pharmacology analysis identified three active components of CKI and 13 key targets. Molecular docking analysis showed that TNF, PTEN, CCND1, MAPK3, IL6, HIF1A, MYC had high affinity with corresponding components. Then the key pathway, cell cycle and the core targets MYC, CCND1, and P15 related to the key pathway were obtained. The results of in vitro experiments showed that CKI could inhibit the proliferation, migration, and invasion of NPC 5-8F cells and C666-1 cells, induce apoptosis of C666-1 cells, and arrest cell cycle G0/G1 phase. In addition, RT-qPCR and western blot showed that the expression of P15 was up-regulated and E2F4, E2F5, c-Myc, CCND1, and P107 was down-regulated in 5-8F cells and C666-1 cells intervened by CKI. Conclusion: The key pathway, cell cycle and the corresponding core targets MYC, CCND1, and P15 were obtained from network pharmacology, molecular docking, and proteomics. CKI could inhibit the proliferation, migration, and invasion of NPC cells, induce apoptosis of C666-1 cells. Especially CKI may arrest cell cycle G0/G1 phase through regulating targets MYC/P15/CCND1 of cell cycle pathway.
MeSH term(s)	Humans ; Nasopharyngeal Carcinoma/drug therapy ; Molecular Docking Simulation ; Antineoplastic Agents/pharmacology ; Drugs, Chinese Herbal/pharmacology ; Signal Transduction ; Nasopharyngeal Neoplasms/drug therapy ; Cyclin D1/genetics
Chemical Substances	kushen (IYR6K8KQ5K) ; Antineoplastic Agents ; Drugs, Chinese Herbal ; CCND1 protein, human ; Cyclin D1 (136601-57-5)
Language	English
Publishing date	2023-05-29
Publishing country	Ireland
Document type	Journal Article
ZDB-ID	134511-4
ISSN	1872-7573 ; 0378-8741
ISSN (online)	1872-7573
ISSN	0378-8741
DOI	10.1016/j.jep.2023.116702
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Article ; Online: Elucidating the pharmacological effects of Compound Kushen injection on MYC-P15-CCND1 signaling pathway in nasopharyngeal carcinoma - An in vitro study

Journal of Ethnopharmacology. 2023 May 29, p.116702-

2023 , Page(s) 116702–

Abstract: Compound Kushen injection (CKI) is a representative medication of Chinese herbal injection and is often used in the adjuvant treatment of nasopharyngeal carcinoma (NPC), but its antitumor mechanism is poorly understood. To preliminarily elucidate the ... ...

Abstract	Compound Kushen injection (CKI) is a representative medication of Chinese herbal injection and is often used in the adjuvant treatment of nasopharyngeal carcinoma (NPC), but its antitumor mechanism is poorly understood. To preliminarily elucidate the effects and possible mechanisms of CKI on NPC. In this work, we explored the possible molecular mechanisms of CKI against NPC by using network pharmacology and molecular docking. In addition, proteomics was used to explore the localization and quantitative information of protein in NPC C666-1 cells after the intervention of CKI, and enrichment analysis was used to obtain the potential targets and pathways. Finally, the effect and the core targets of CKI in the intervention of NPC were explored in vitro experiments. Network pharmacology analysis identified three active components of CKI and 13 key targets. Molecular docking analysis showed that TNF, PTEN, CCND1, MAPK3, IL6, HIF1A, MYC had high affinity with corresponding components. Then the key pathway, cell cycle and the core targets MYC, CCND1, and P15 related to the key pathway were obtained. The results of in vitro experiments showed that CKI could inhibit the proliferation, migration, and invasion of NPC 5–8F cells and C666-1 cells, induce apoptosis of C666-1 cells, and arrest cell cycle G0/G1 phase. In addition, RT-qPCR and western blot showed that the expression of P15 was up-regulated and E2F4, E2F5, c-Myc, CCND1, and P107 was down-regulated in 5–8F cells and C666-1 cells intervened by CKI. The key pathway, cell cycle and the corresponding core targets MYC, CCND1, and P15 were obtained from network pharmacology, molecular docking, and proteomics. CKI could inhibit the proliferation, migration, and invasion of NPC cells, induce apoptosis of C666-1 cells. Especially CKI may arrest cell cycle G0/G1 phase through regulating targets MYC/P15/CCND1 of cell cycle pathway.
Keywords	Western blotting ; adjuvants ; apoptosis ; carcinoma ; cell cycle ; drug therapy ; interleukin-6 ; pharmacology ; proteomics ; traditional medicine ; Nasopharyngeal carcinoma ; Compound Kushen injection ; Network pharmacology ; Molecular docking ; Experimental evaluation
Language	English
Dates of publication	2023-0529
Publishing place	Elsevier B.V.
Document type	Article ; Online
Note	Pre-press version
ZDB-ID	134511-4
ISSN	1872-7573 ; 0378-8741
ISSN (online)	1872-7573
ISSN	0378-8741
DOI	10.1016/j.jep.2023.116702
Database	NAL-Catalogue (AGRICOLA)

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Article ; Online: Compound Kushen Injection inhibits epithelial-mesenchymal transition of gastric carcinoma by regulating VCAM1 induced by the TNF signaling pathway

Huang, Zhihong / Wu, Chao / Zhou, Wei / Lu, Shan / Tan, Yingying / Wu, Zhishan / You, Rongli / Stalin, Antony / Fengzhongyiying / Zhang, Jingyuan / Liu, Pengyun / Wang, Wei / Duan, Xiaoxia / You, Leiming / Wu, Jiarui

Phytomedicine. 2023 July 17, p.154984-

2023 , Page(s) 154984–

Abstract: Gastric carcinoma (GC) treatment needs to be developed rapidly. Compound Kushen Injection (CKI), a formula from traditional Chinese medicine, has been used clinically in combination with chemotherapy to treat GC with satisfactory results. However, the ... ...

Abstract	Gastric carcinoma (GC) treatment needs to be developed rapidly. Compound Kushen Injection (CKI), a formula from traditional Chinese medicine, has been used clinically in combination with chemotherapy to treat GC with satisfactory results. However, the molecular mechanism by which CKI acts to cure GC is still unclear. In the present study, in vivo and in vitro experiments were used to assess the efficacy of CKI. Using ceRNA microarray and TMT technologies, the molecular mechanism of CKI was further investigated at the transcriptional and protein levels, and a bioinformatics approach was employed to investigate and functionally validate key CKI targets in GC. When combined with cisplatin (DDP), CKI significantly increased its efficacy in preventing the proliferation and metastasis of GC cells and malignant-looking tumors in mice. High-throughput sequencing data and bioinformatics analysis showed that CKI regulated the TNF signaling pathway, epithelial-mesenchymal transition (EMT), with VCAM1 as a key target. The transcription factors CEBPB, JUN, RELA, NFKB1, the EMT mesenchymal-like cell markers N-cadherin and vimentin, as well as the expression of VCAM1 and its upstream signaling driver TNF, were all downregulated by CKI. In contrast, the expression of the EMT epithelial-like cell marker E-cadherin was upregulated. CKI can effectively inhibit GC growth and metastasis, improve body's immunity, and protect normal tissues from damage. The molecular mechanism by which CKI inhibits metastasis of GC is by regulating VCAM1 induced by the TNF signaling pathway to inhibit EMT of GC. Our results provide an important clue to clarify precisely the multi-scale molecular mechanism of CKI in the treatment of GC.
Keywords	Oriental traditional medicine ; bioinformatics ; cadherins ; carcinoma ; cisplatin ; drug therapy ; immunity ; metastasis ; microarray technology ; transcription (genetics) ; vimentin ; Compound Kushen Injection ; Epithelial-mesenchymal transition ; Gastric carcinoma ; High-throughput sequencing ; Vascular cell adhesion molecule 1 ; CAM ; CDH1 ; CDH2 ; CEBPB ; CKI ; DDP ; DEG ; DEP ; EMT ; GC ; JUN ; NFKB1 ; RELA ; STAD ; TF ; TNF ; VCAM1 ; VIM
Language	English
Dates of publication	2023-0717
Publishing place	Elsevier GmbH
Document type	Article ; Online
Note	Pre-press version
ZDB-ID	1205240-1
ISSN	1618-095X ; 0944-7113
ISSN (online)	1618-095X
ISSN	0944-7113
DOI	10.1016/j.phymed.2023.154984
Database	NAL-Catalogue (AGRICOLA)

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Article ; Online: The anti-hepatocellular carcinoma effect of Aidi injection was related to the synergistic action of cantharidin, formononetin, and isofraxidin through BIRC5, FEN1, and EGFR.

Lu, Shan / Huang, Jiaqi / Zhang, Jingyuan / Wu, Chao / Huang, Zhihong / Tao, Xiaoyu / You, Leiming / Stalin, Antony / Chen, Meilin / Li, Jiaqi / Tan, Yingying / Wu, Zhishan / Geng, Libo / Li, Zhiqi / Fan, Qiqi / Liu, Pengyun / Lin, Yifan / Zhao, Chongjun / Wu, Jiarui

Journal of ethnopharmacology

2023 Volume 319, Issue Pt 2, Page(s) 117209

Abstract: Ethnopharmacological relevance: Aidi injection (ADI) is a popular anti-tumor Chinese patent medicine, widely used in clinics for the treatment of hepatocellular carcinoma (HCC) with remarkable therapeutic effects through multiple targets and pathways. ... ...

Abstract	Ethnopharmacological relevance: Aidi injection (ADI) is a popular anti-tumor Chinese patent medicine, widely used in clinics for the treatment of hepatocellular carcinoma (HCC) with remarkable therapeutic effects through multiple targets and pathways. However, the scientific evidence of the synergistic role of the complex chemical component system and the potential mechanism for treating diseases are ignored and remain to be elucidated. Aim of the study: This study aimed to elucidate and verify the cooperative association between the potential active ingredient of ADI, which is of significance to enlarge our understanding of its anti-HCC molecular mechanisms. Materials and methods: Firstly, the anti-HCC effect of ADI was evaluated in various HCC cells and the zebrafish xenograft model. Subsequently, a variety of bioinformatic technologies, including network pharmacology, weighted gene co-expression network analysis (WGCNA), meta-analysis of gene expression profiles, and pathway enrichment analysis were performed to construct the competitive endogenous RNA (ceRNA) network of ADI intervention in HCC and to establish the relationship between the critical targets/pathways and the key corresponding components, which were involved in ADI against HCC in a synergistic way and were validated by molecular biology experiments. Results: ADI exerted remarkable anti-HCC in vitro cells and in vivo zebrafish model, especially that the Hep 3B2.1-7 cell showed substantial sensibility to ADI. The ceRNA network revealed that the EGFR/PI3K/AKT signaling pathway was identified as the promising pathway. Furthermore, the meta-analysis also demonstrated the critical role of BIRC5 and FEN1 as key targets. Finally, the synergistic effect of ADI was revealed by discovering the inhibitory effect of cantharidin on BIRC5, formononetin on FEN1 and EGFR, as well as isofraxidin on EGFR. Conclusion: Our study unveiled that the incredible protective effect of ADI on HCC resulted from the synergistic inhibition effect of cantharidin, formononetin, and isofraxidin on multiple targets/pathways, including BIRC5, FEN1, and EGFR/PI3K/AKT, respectively, providing a scientific interpretation of ADI against HCC and a typical example of pharmacodynamic evaluation of other proprietary Chinese patent medicine.
MeSH term(s)	Humans ; Animals ; Carcinoma, Hepatocellular/drug therapy ; Carcinoma, Hepatocellular/genetics ; Cantharidin ; Zebrafish ; Phosphatidylinositol 3-Kinases ; Proto-Oncogene Proteins c-akt ; Liver Neoplasms/drug therapy ; Nonprescription Drugs ; ErbB Receptors/genetics ; Flap Endonucleases ; Survivin/genetics
Chemical Substances	formononetin (295DQC67BJ) ; isofraxidin (304915F056) ; Cantharidin (IGL471WQ8P) ; Phosphatidylinositol 3-Kinases (EC 2.7.1.-) ; Proto-Oncogene Proteins c-akt (EC 2.7.11.1) ; Nonprescription Drugs ; ErbB Receptors (EC 2.7.10.1) ; FEN1 protein, human (EC 3.1.11.-) ; Flap Endonucleases (EC 3.1.-) ; BIRC5 protein, human ; Survivin ; EGFR protein, human (EC 2.7.10.1)
Language	English
Publishing date	2023-09-25
Publishing country	Ireland
Document type	Meta-Analysis ; Journal Article
ZDB-ID	134511-4
ISSN	1872-7573 ; 0378-8741
ISSN (online)	1872-7573
ISSN	0378-8741
DOI	10.1016/j.jep.2023.117209
Database	MEDical Literature Analysis and Retrieval System OnLINE

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