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Article: Preparation of osteogenic matrices from cultured cells.

Gregory, Carl A / McNeill, Eoin P / Pan, Simin

2019 Volume 156, Page(s) 15–43

Abstract: Bone is a composite material consisting primarily of cells, extracellular matrices, accessory proteins and the complex calcium phosphate salt hydroxyapatite. Collectively, the extracellular network of proteins and accessory molecules that provide the ... ...

Abstract	Bone is a composite material consisting primarily of cells, extracellular matrices, accessory proteins and the complex calcium phosphate salt hydroxyapatite. Collectively, the extracellular network of proteins and accessory molecules that provide the organic component of bone tissue is referred to as the osteogenic extracellular matrix (OECM). OECM provides tensile strength and increases the durability of bone, but the OECM also serves as an attachment site and regulatory substrate for cells and a repository for growth factors and cytokines. Increasingly, purified OECM generated by osteogenic cells in culture has attracted interest because it has the capacity to improve the growth and viability of attached cells, enhances the osteogenic program in vitro and in vivo, and shows great promise as a therapeutic tool for orthopedic tissue engineering. This chapter will describe fundamental protocols for the selection and culture of osteogenic cells and conditions for their osteogenic differentiation, and the synthesis, purification and characterization of OECM. Some examples of immobilization to surfaces for the purpose of two- and three-dimensional culture will also be described.
MeSH term(s)	Alkaline Phosphatase/metabolism ; Animals ; Biomarkers/metabolism ; Calcification, Physiologic ; Cell Adhesion ; Cells, Cultured ; Extracellular Matrix/metabolism ; Extracellular Matrix/ultrastructure ; Humans ; Mesenchymal Stem Cells/cytology ; Osteogenesis ; Swine ; Tissue Engineering/methods
Chemical Substances	Biomarkers ; Alkaline Phosphatase (EC 3.1.3.1)
Language	English
Publishing date	2019-12-10
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ISSN	0091-679X
ISSN	0091-679X
DOI	10.1016/bs.mcb.2019.10.009
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article: Huang Qin Decoction inhibits the initiation of experimental colitis associated carcinogenesis by controlling the PAD4 dependent NETs

Pan, Zengfeng / Xie, Xuting / Chen, Yunliang / Pan, Simin / Wu, Zhiyun / Yang, Caiyi / Liang, Junjie / Zhang, Meilin / Wang, Qing / Chen, Jinyan / Zhou, Lian / Luo, Xia

Phytomedicine. 2022 Dec., v. 107

2022

Abstract: Colorectal cancer is associated with ulcerative colitis (UC). The infiltration of neutrophils is the main cause of DNA damage produced by inflammation in the intestinal epithelium. Under the action of peptidyl arginine deaminase 4 (PAD4), neutrophils ... ...

Abstract	Colorectal cancer is associated with ulcerative colitis (UC). The infiltration of neutrophils is the main cause of DNA damage produced by inflammation in the intestinal epithelium. Under the action of peptidyl arginine deaminase 4 (PAD4), neutrophils dissociate chromatin and form neutrophil extracellular traps (NETs), which can aggravate tissue inflammation and encourage tumor development. Although Huang Qin Decoction (HQD) was found to be useful in treating UC and was used to gradually prevent and treat digestive tract cancers, the underlying reasons were unclear. To demonstrate HQD could inhibits the initiation of colitis associated carcinogenesis by controlling NETs related inflammation, we first performed an AOM/DSS-generated colitis-associated carcinogenesis model to assess the efficacy of HQD in reducing neutrophil infiltration and anti-tumor activity. Then, using network pharmacology research, we investigated the potential mechanisms underlying those medicinal effects, as demonstrated by the detection of NETs aggregation and PAD4 expression changes in the colon. HQD substantially reduced the number of colon cancers and the expression of Ki67, restored the level of intestinal tight junction protein occludin and ZO-1, and relieved the intestinal inflammation caused by TNF-α, IL-1β. At the same time, it inhibited neutrophil infiltration in the colon and improved the immunosurveillance of CD8⁺T cells. The potential mechanisms of HQD intervention against UC and UC with neoplasia (UCN) were studied using network pharmacology, and 156 conjunct genes as well as numerous inflammation-related pathways were identified. Protein-protein interaction (PPI) analysis indicated that HQD inhibition of intestinal tumors might be related to the deactivation of PAD4, which was verified by the down-regulation of NETs, MPO-DNA complex levels, and PAD4 expression after HQD treatment. Huang Qin Decoction inhibits the initiation of colitis associated carcinogenesis by controlling PAD4-dependent neutrophil extracellular traps.
Keywords	DNA damage ; antineoplastic activity ; arginine ; carcinogenesis ; chromatin ; colon ; colorectal neoplasms ; digestive tract ; inflammation ; intestinal mucosa ; models ; neutrophils ; occludins ; protein-protein interactions ; tight junctions ; ulcerative colitis
Language	English
Dates of publication	2022-12
Publishing place	Elsevier GmbH
Document type	Article
ZDB-ID	1205240-1
ISSN	1618-095X ; 0944-7113
ISSN (online)	1618-095X
ISSN	0944-7113
DOI	10.1016/j.phymed.2022.154454
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Article ; Online: Quercetin ameliorates ulcerative colitis by activating aryl hydrocarbon receptor to improve intestinal barrier integrity.

Wang, Xiaojing / Xie, Xuting / Li, Yanyang / Xie, Xueqian / Huang, Shaowei / Pan, Simin / Zou, Yanling / Pan, Zengfeng / Wang, Qing / Chen, Jinyan / Zhou, Lian / Luo, Xia

Phytotherapy research : PTR

2023 Volume 38, Issue 1, Page(s) 253–264

Abstract: Ulcerative colitis (UC) pathogenesis is largely associated with intestinal epithelial barrier dysfunction. A therapeutic approach to UC involves the repair of damaged intestinal barrier. Our study aimed to investigate whether aryl hydrocarbon receptor ( ... ...

Abstract	Ulcerative colitis (UC) pathogenesis is largely associated with intestinal epithelial barrier dysfunction. A therapeutic approach to UC involves the repair of damaged intestinal barrier. Our study aimed to investigate whether aryl hydrocarbon receptor (AhR) mediated the intestinal barrier repair effects of quercetin to ameliorate UC. 3% dextran sulfate sodium was used to induce colitic mice, and quercetin (25, 50, and 100 mg/kg) was administered orally for 10 days to assess the therapeutic effects. In vitro, Caco-2 cells were used to explore the effect of quercetin on tight junction protein expression and AhR activation. The results showed that quercetin alleviated colitic mice by restoring tight junctions (TJs) integrity via an AhR-dependent manner (p < 0.05). In vitro, quercetin dose-dependently elevated the expressions of TJs protein ZO-1 and Claudin1, and activated AhR by enhancing the expression of CYP1A1 and facilitating AhR nuclear translocation in Caco-2 cells (p < 0.05). While AhR antagonist CH223191 reversed the therapeutic effects of quercetin (p < 0.05) and blocked quercetin-induced AhR activation and enhancement of TJs protein (p < 0.05). In conclusion, quercetin repaired intestinal barrier dysfunction by activating AhR-mediated enhancement of TJs to alleviate UC. Our research offered new perspectives on how quercetin enhanced intestinal barrier function.
MeSH term(s)	Humans ; Animals ; Mice ; Colitis, Ulcerative/chemically induced ; Colitis, Ulcerative/drug therapy ; Colitis, Ulcerative/pathology ; Caco-2 Cells ; Quercetin/pharmacology ; Quercetin/therapeutic use ; Receptors, Aryl Hydrocarbon/metabolism ; Receptors, Aryl Hydrocarbon/therapeutic use ; Intestines ; Colitis/chemically induced ; Dextran Sulfate/adverse effects ; Mice, Inbred C57BL ; Intestinal Mucosa ; Disease Models, Animal
Chemical Substances	Quercetin (9IKM0I5T1E) ; Receptors, Aryl Hydrocarbon ; Dextran Sulfate (9042-14-2)
Language	English
Publishing date	2023-10-23
Publishing country	England
Document type	Journal Article
ZDB-ID	639136-9
ISSN	1099-1573 ; 0951-418X
ISSN (online)	1099-1573
ISSN	0951-418X
DOI	10.1002/ptr.8027
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Article ; Online: Baitouweng decoction repairs the intestinal barrier in DSS-induced colitis mice via regulation of AMPK/mTOR-mediated autophagy

Pan, Si-Min / Hu, Zhi-Fan / Wang, Chun-Li / Tiu, Cheryl / Pan, Zeng-Feng / Zhou, Ruo-Yu / Wang, Xiao-Jing / Huang, Shao-Wei / Li, Yan-Yang / Wang, Qing / Luo, Xia / Zhou, Lian / Hou, Jiang-Tao / Chen, Bin

Journal of Ethnopharmacology. 2023 July 10, p.116888-

2023 , Page(s) 116888–

Abstract: Ulcerative colitis (UC) is one of non-specific inflammatory bowel disease that mainly affects the colon. Recently, UC has become a significant social and economic problem worldwide. Baitouweng decoction (BD), a traditional Chinese medicine described in ... ...

Abstract	Ulcerative colitis (UC) is one of non-specific inflammatory bowel disease that mainly affects the colon. Recently, UC has become a significant social and economic problem worldwide. Baitouweng decoction (BD), a traditional Chinese medicine described in the “Treatise on Febrile Diseases”, has been used for centuries to treat intestinal diseases. However, its underlying mechanism remains largely unexplored. In this study, we aimed to investigate the effect of BD on autophagy for repairing the colonic barrier in DSS-induced colitis mice and explored its role in regulating the autophagic signaling pathway AMPK/mTOR. Mice with colitis were treated with 3% dextran sulfate sodium (DSS) for 7 days. The effectiveness of BD in treating DSS-induced colitis was evaluated through body weight, disease activity index (DAI), colon length, pathological changes, organ index, and proportion of blood cells. Moreover, intestinal epithelial permeability was analyzed by examining FITC-dextran leakage, the bacterial load of mesenteric lymph nodes (MLNs), and bacterial infiltration of colon tissues. Barrier function was evaluated by assessing the number and proportion of colonic goblet cells and the expression of tight junction proteins, including ZO-1, claudin-1, and occludin. Furthermore, the levels of autophagy were assessed by examining the number of autophagosomes and the expression of the autophagy-related proteins LC3, Beclin1, and P62. Additionally, network pharmacology research was conducted to analyze the potential mechanisms underlying the medicinal effects, as indicated by the role of AMPK/mTOR in regulating the autophagic signaling pathway. BD improved colitis symptoms in mice by restoring body weight and colon length and reducing inflammatory cell infiltration. Additionally, BD decreased the diffusion of FITC-dextran and bacterial translocation in MLNs, as well as bacterial infiltration of the colonic mucosa. The number and proportion of colonic goblet cells, the expression of ZO-1, Claudin-1, and Occludin, and the levels of autophagy were also increased by BD. Network pharmacology analysis suggested that BD might affect intestinal autophagy through the AMPK signaling pathway, which was confirmed by the activation of AMPK phosphorylation and the downregulation of mTOR expression following BD treatment. Our study demonstrated that BD repaired the intestinal epithelial barrier in DSS-induced colitis mice by activating AMPK phosphorylation and inhibiting mTOR expression to promote autophagy.
Keywords	Oriental traditional medicine ; autophagosomes ; autophagy ; blood ; body weight ; colon ; dextran sulfate ; lymph ; microbial load ; mucosa ; occludins ; permeability ; pharmacology ; phosphorylation ; tight junctions ; ulcerative colitis ; Baitouweng decoction ; Colitis ; Intestinal barrier ; Tight junction ; AMPK/mTOR ; AMPK ; BD ; DAI ; FITC-dextran ; GO ; H&E ; HGB ; JAMs ; KEGG ; MLNs ; mTOR ; RBC ; TEM ; TJs ; UC ; WBC
Language	English
Dates of publication	2023-0710
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.2023.116888
Database	NAL-Catalogue (AGRICOLA)

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Article ; Online: Baitouweng decoction repairs the intestinal barrier in DSS-induced colitis mice via regulation of AMPK/mTOR-mediated autophagy.

Pan, Si-Min / Wang, Chun-Li / Hu, Zhi-Fan / Zhang, Mei-Ling / Pan, Zeng-Feng / Zhou, Ruo-Yu / Wang, Xiao-Jing / Huang, Shao-Wei / Li, Yan-Yang / Wang, Qing / Luo, Xia / Zhou, Lian / Hou, Jiang-Tao / Chen, Bin

Journal of ethnopharmacology

2023 Volume 318, Issue Pt A, Page(s) 116888

Abstract: Ethnopharmacological relevance: Ulcerative colitis (UC) is one of non-specific inflammatory bowel disease that mainly affects the colon. Recently, UC has become a significant social and economic problem worldwide. Baitouweng decoction (BD), a ... ...

Abstract	Ethnopharmacological relevance: Ulcerative colitis (UC) is one of non-specific inflammatory bowel disease that mainly affects the colon. Recently, UC has become a significant social and economic problem worldwide. Baitouweng decoction (BD), a traditional Chinese medicine described in the "Treatise on Febrile Diseases", has been used for centuries to treat intestinal diseases. However, its underlying mechanism remains largely unexplored. Aim of study: In this study, we aimed to investigate the effect of BD on autophagy for repairing the colonic barrier in DSS-induced colitis mice and explored its role in regulating the autophagic signaling pathway AMPK/mTOR. Materials and methods: Mice with colitis were treated with 3% dextran sulfate sodium (DSS) for 7 days. The effectiveness of BD in treating DSS-induced colitis was evaluated through body weight, disease activity index (DAI), colon length, pathological changes, organ index, and proportion of blood cells. Moreover, intestinal epithelial permeability was analyzed by examining FITC-dextran leakage, the bacterial load of mesenteric lymph nodes (MLNs), and bacterial infiltration of colon tissues. Barrier function was evaluated by assessing the number and proportion of colonic goblet cells and the expression of tight junction proteins, including ZO-1, claudin-1, and occludin. Furthermore, the levels of autophagy were assessed by examining the number of autophagosomes and the expression of the autophagy-related proteins LC3, Beclin1, and P62. Additionally, network pharmacology research was conducted to analyze the potential mechanisms underlying the medicinal effects, as indicated by the role of AMPK/mTOR in regulating the autophagic signaling pathway. Results: BD improved colitis symptoms in mice by restoring body weight and colon length and reducing inflammatory cell infiltration. Additionally, BD decreased the diffusion of FITC-dextran and bacterial translocation in MLNs, as well as bacterial infiltration of the colonic mucosa. The number and proportion of colonic goblet cells, the expression of ZO-1, Claudin-1, and Occludin, and the levels of autophagy were also increased by BD. Network pharmacology analysis suggested that BD might affect intestinal autophagy through the AMPK signaling pathway, which was confirmed by the activation of AMPK phosphorylation and the downregulation of mTOR expression following BD treatment. Conclusion: Our study demonstrated that BD repaired the intestinal epithelial barrier in DSS-induced colitis mice by activating AMPK phosphorylation and inhibiting mTOR expression to promote autophagy.
MeSH term(s)	Mice ; Animals ; AMP-Activated Protein Kinases/metabolism ; Occludin/metabolism ; Claudin-1/metabolism ; Colitis/chemically induced ; Colitis/drug therapy ; Colitis/metabolism ; Colitis, Ulcerative/chemically induced ; Colitis, Ulcerative/drug therapy ; Colitis, Ulcerative/pathology ; Colon ; TOR Serine-Threonine Kinases/metabolism ; Intestinal Mucosa ; Autophagy ; Body Weight ; Dextran Sulfate/toxicity ; Disease Models, Animal ; Mice, Inbred C57BL
Chemical Substances	fluorescein isothiocyanate dextran ; AMP-Activated Protein Kinases (EC 2.7.11.31) ; Occludin ; Claudin-1 ; TOR Serine-Threonine Kinases (EC 2.7.11.1) ; Dextran Sulfate (9042-14-2)
Language	English
Publishing date	2023-07-10
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.2023.116888
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Article: Sphingosine-1-Phosphate Alleviates Irradiation Induced Salivary Gland Hypofunction through Preserving Endothelial Cells and Resident Macrophages.

Yang, Tao / Zhao, Qingguo / Hu, Meijun / Pan, Simin / Zhang, Linying / Zhu, Ruoxi / Zhou, Bowen / Feng, Xuanhe / Gao, Zhenhua / Zhu, Zhao / Zhang, Yu / Hu, Liang / Liu, Fei / Shan, Zhaochen

Antioxidants (Basel, Switzerland)

2022 Volume 11, Issue 10

Abstract: Radiotherapy for head-and-neck cancers frequently causes long-term hypofunction of salivary glands that severely compromises quality of life and is difficult to treat. Here, we studied effects and mechanisms of Sphingosine-1-phosphate (S1P), a versatile ... ...

Abstract	Radiotherapy for head-and-neck cancers frequently causes long-term hypofunction of salivary glands that severely compromises quality of life and is difficult to treat. Here, we studied effects and mechanisms of Sphingosine-1-phosphate (S1P), a versatile signaling sphingolipid, in preventing irreversible dry mouth caused by radiotherapy. Mouse submandibular glands (SMGs) were irradiated with or without intra-SMG S1P pretreatment. The saliva flow rate was measured following pilocarpine stimulation. The expression of genes related to S1P signaling and radiation damage was examined by flow cytometry, immunohistochemistry, quantitative RT-PCR, Western blotting, and/or single-cell RNA-sequencing. S1P pretreatment ameliorated irradiation-induced salivary dysfunction in mice through a decrease in irradiation-induced oxidative stress and consequent apoptosis and cellular senescence, which is related to the enhancement of Nrf2-regulated anti-oxidative response. In mouse SMGs, endothelial cells and resident macrophages are the major cells capable of producing S1P and expressing the pro-regenerative S1P receptor S1pr1. Both mouse SMGs and human endothelial cells are protected from irradiation damage by S1P pretreatment, likely through the S1pr1/Akt/eNOS axis. Moreover, intra-SMG-injected S1P did not affect the growth and radiosensitivity of head-and-neck cancer in a mouse model. These data indicate that S1P signaling pathway is a promising target for alleviating irradiation-induced salivary gland hypofunction.
Language	English
Publishing date	2022-10-18
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2704216-9
ISSN	2076-3921
ISSN	2076-3921
DOI	10.3390/antiox11102050
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Article ; Online: Dahuang Mudan decoction repairs intestinal barrier in chronic colitic mice by regulating the function of ILC3.

Huang, Shaowei / Wang, Xiaojing / Xie, Xueqian / Su, Yulin / Pan, Zengfeng / Li, Yanyang / Liang, Junjie / Zhang, Meiling / Pan, Simin / Xu, Bo / Li, Linzhu / Chen, Jinyan / Luo, Xia / Zhou, Lian

Journal of ethnopharmacology

2022 Volume 299, Page(s) 115652

Abstract: Ethnopharmacological relevance: Dahuang Mudan decoction (DMD) is a classic prescription for treating intestinal carbuncle from Zhang Zhongjing's "Essentials of the Golden Chamber" in the Han Dynasty. Recent studies also prove that DMD has a therapeutic ... ...

Abstract	Ethnopharmacological relevance: Dahuang Mudan decoction (DMD) is a classic prescription for treating intestinal carbuncle from Zhang Zhongjing's "Essentials of the Golden Chamber" in the Han Dynasty. Recent studies also prove that DMD has a therapeutic effect on ulcerative colitis (UC), but its mechanism is still unclear. Aim of study: In this study, we aim to assess the therapeutic effect of DMD on DSS-induced chronic colitis in mice and deeply expound its underlying regulative mechanism. Materials and methods: The efficacy of DMD on mice with 2% DSS-induced chronic colitis was examined by changes in mouse body weight, DAI score, colon length changes, peripheral blood white blood cells (WBC) and red blood cells (RBC) counts, and hemoglobin (HGB) content, using mesalazine as a positive control. A small animal imaging system observed the FITC-Dextran fluorescence distribution in mice, and the contents of IL-22 and IL-17A in colon tissue homogenate supernatant and LPS in peripheral blood were detected by ELISA. Fluorescence in situ molecular hybridization and bacterial culture were used to investigate bacterial infiltration in intestinal mucosa and bacterial translocation in mesenteric lymph nodes and spleen. Mice immune function was further evaluated by analyzing the changes in spleen index, thymus index, and the ratio of peripheral blood granulocytes, monocytes, and lymphocytes. Meanwhile, the proportion of NCR Results: DMD restored the body weight, colon length, peripheral blood RBC numbers, and HGB content of chronic colitis mice and reduced peripheral blood WBC and colon inflammatory cell infiltration. Moreover, DMD decreased LPS content in serum, bacterial infiltration of colonic mucosa, and bacterial translocation in spleen and mesenteric lymph nodes. Simultaneously, DMD intensified the expression of ZO-1, Occludin, and Claudin-1, the ratio of NCR Conclusion: Our results confirm that DMD improves inflammation and restores intestinal epithelial function in mice with chronic colitis, and the mechanism may be related to regulating ILC3 function.
MeSH term(s)	Animals ; Body Weight ; Caco-2 Cells ; Claudin-1/metabolism ; Colitis/chemically induced ; Colitis/drug therapy ; Colitis/metabolism ; Colitis, Ulcerative/chemically induced ; Colitis, Ulcerative/drug therapy ; Colitis, Ulcerative/pathology ; Culture Media, Conditioned/adverse effects ; Culture Media, Conditioned/metabolism ; Dextran Sulfate ; Disease Models, Animal ; Granulocyte-Macrophage Colony-Stimulating Factor ; Humans ; Immunity, Innate ; Interleukin-17/metabolism ; Intestinal Mucosa/metabolism ; Lipopolysaccharides/pharmacology ; Lymphocytes/metabolism ; Mesalamine/adverse effects ; Mice ; Mice, Inbred C57BL ; Occludin/metabolism ; Tight Junction Proteins/metabolism
Chemical Substances	Claudin-1 ; Culture Media, Conditioned ; Interleukin-17 ; Lipopolysaccharides ; Occludin ; Tight Junction Proteins ; Mesalamine (4Q81I59GXC) ; Granulocyte-Macrophage Colony-Stimulating Factor (83869-56-1) ; Dextran Sulfate (9042-14-2)
Language	English
Publishing date	2022-08-28
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.2022.115652
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Article ; Online: Huang Qin Decoction inhibits the initiation of experimental colitis associated carcinogenesis by controlling the PAD4 dependent NETs.

Pan, Zengfeng / Xie, Xuting / Chen, Yunliang / Pan, Simin / Wu, Zhiyun / Yang, Caiyi / Liang, Junjie / Zhang, Meilin / Wang, Qing / Chen, Jinyan / Zhou, Lian / Luo, Xia

Phytomedicine : international journal of phytotherapy and phytopharmacology

2022 Volume 107, Page(s) 154454

Abstract: Background: Colorectal cancer is associated with ulcerative colitis (UC). The infiltration of neutrophils is the main cause of DNA damage produced by inflammation in the intestinal epithelium. Under the action of peptidyl arginine deaminase 4 (PAD4), ... ...

Abstract	Background: Colorectal cancer is associated with ulcerative colitis (UC). The infiltration of neutrophils is the main cause of DNA damage produced by inflammation in the intestinal epithelium. Under the action of peptidyl arginine deaminase 4 (PAD4), neutrophils dissociate chromatin and form neutrophil extracellular traps (NETs), which can aggravate tissue inflammation and encourage tumor development. Although Huang Qin Decoction (HQD) was found to be useful in treating UC and was used to gradually prevent and treat digestive tract cancers, the underlying reasons were unclear. Methods: To demonstrate HQD could inhibits the initiation of colitis associated carcinogenesis by controlling NETs related inflammation, we first performed an AOM/DSS-generated colitis-associated carcinogenesis model to assess the efficacy of HQD in reducing neutrophil infiltration and anti-tumor activity. Then, using network pharmacology research, we investigated the potential mechanisms underlying those medicinal effects, as demonstrated by the detection of NETs aggregation and PAD4 expression changes in the colon. Results: HQD substantially reduced the number of colon cancers and the expression of Ki67, restored the level of intestinal tight junction protein occludin and ZO-1, and relieved the intestinal inflammation caused by TNF-α, IL-1β. At the same time, it inhibited neutrophil infiltration in the colon and improved the immunosurveillance of CD8 Conclusion: Huang Qin Decoction inhibits the initiation of colitis associated carcinogenesis by controlling PAD4-dependent neutrophil extracellular traps.
MeSH term(s)	Animals ; Arginine/metabolism ; Carcinogenesis ; Chromatin/metabolism ; Colitis/chemically induced ; Colitis/complications ; Colitis/drug therapy ; Colitis, Ulcerative/chemically induced ; Colitis, Ulcerative/drug therapy ; Disease Models, Animal ; Extracellular Traps/metabolism ; Humans ; Inflammation/metabolism ; Ki-67 Antigen/metabolism ; Mice ; Mice, Inbred C57BL ; Occludin/metabolism ; Scutellaria baicalensis ; Tumor Necrosis Factor-alpha/metabolism
Chemical Substances	Chromatin ; Ki-67 Antigen ; Occludin ; Tumor Necrosis Factor-alpha ; Arginine (94ZLA3W45F)
Language	English
Publishing date	2022-09-11
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.2022.154454
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Article ; Online: Morpholino-driven blockade of Dkk-1 in osteosarcoma inhibits bone damage and tumour expansion by multiple mechanisms.

Pan, Simin / Cesarek, Michael / Godoy, Carla / Co, Cynthia M / Schindler, Catherine / Padilla, Kelbi / Haskell, Andrew / Barreda, Heather / Story, Christopher / Poole, Roy / Dabney, Alan / Gregory, Carl A

British journal of cancer

2022 Volume 127, Issue 1, Page(s) 43–55

Abstract: Background: Osteosarcoma (OS) is the most common primary bone malignancy. Chemotherapy plays an essential role in OS treatment, potentially doubling 5-year event-free survival if tumour necrosis can be stimulated. The canonical Wnt inhibitor Dickkopf-1 ( ...

Abstract	Background: Osteosarcoma (OS) is the most common primary bone malignancy. Chemotherapy plays an essential role in OS treatment, potentially doubling 5-year event-free survival if tumour necrosis can be stimulated. The canonical Wnt inhibitor Dickkopf-1 (Dkk-1) enhances OS survival in part through upregulation of aldehyde-dehydrogenase-1A1 which neutralises reactive oxygen species originating from nutritional stress and chemotherapeutic challenge. Methods: A vivo morpholino (DkkMo) was employed to block the expression of Dkk-1 in OS cells. Cell mitosis, gene expression and bone destruction were measured in vitro and in vivo in the presence and absence of doxorubicin (DRB). Results: DkkMo reduced the expression of Dkk-1 and Aldh1a1, reduced expansion of OS tumours, preserved bone volume and architecture and stimulated tumour necrosis. This was observed in the presence or absence of DRB. Conclusion: These results indicate that administration of DkkMo with or without chemotherapeutics can substantially improve OS outcome with respect to tumour expansion and osteolytic corruption of bone in experimental OS model.
MeSH term(s)	Bone Neoplasms/drug therapy ; Bone Neoplasms/genetics ; Bone Neoplasms/metabolism ; Cell Line, Tumor ; Humans ; Intercellular Signaling Peptides and Proteins/genetics ; Morpholinos/genetics ; Morpholinos/pharmacology ; Necrosis ; Osteosarcoma/drug therapy ; Osteosarcoma/genetics ; Osteosarcoma/metabolism
Chemical Substances	Intercellular Signaling Peptides and Proteins ; Morpholinos
Language	English
Publishing date	2022-03-11
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	80075-2
ISSN	1532-1827 ; 0007-0920
ISSN (online)	1532-1827
ISSN	0007-0920
DOI	10.1038/s41416-022-01764-z
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Article: Dahuang Mudan decoction repairs intestinal barrier in chronic colitic mice by regulating the function of ILC3

Huang, Shaowei / Wang, Xiaojing / Xie, Xueqian / Su, Yulin / Pan, Zengfeng / Li, Yanyang / Liang, Junjie / Zhang, Meiling / Pan, Simin / Xu, Bo / Li, Linzhu / Chen, Jinyan / Luo, Xia / Zhou, Lian

Journal of ethnopharmacology. 2022 Aug. 16,

2022

Abstract: Dahuang Mudan decoction (DMD) is a classic prescription for treating intestinal carbuncle from Zhang Zhongjing's “Essentials of the Golden Chamber” in the Han Dynasty. Recent studies also prove that DMD has a therapeutic effect on ulcerative colitis (UC), ...

Abstract	Dahuang Mudan decoction (DMD) is a classic prescription for treating intestinal carbuncle from Zhang Zhongjing's “Essentials of the Golden Chamber” in the Han Dynasty. Recent studies also prove that DMD has a therapeutic effect on ulcerative colitis (UC), but its mechanism is still unclear. In this study, we aim to assess the therapeutic effect of DMD on DSS-induced chronic colitis in mice and deeply expound its underlying regulative mechanism. The efficacy of DMD on mice with 2% DSS-induced chronic colitis was examined by changes in mouse body weight, DAI score, colon length changes, peripheral blood white blood cells (WBC) and red blood cells (RBC) counts, and hemoglobin (HGB) content, using mesalazine as a positive control. A small animal imaging system observed the FITC-Dextran fluorescence distribution in mice, and the contents of IL-22 and IL-17A in colon tissue homogenate supernatant and LPS in peripheral blood were detected by ELISA. Fluorescence in situ molecular hybridization and bacterial culture were used to investigate bacterial infiltration in intestinal mucosa and bacterial translocation in mesenteric lymph nodes and spleen. Mice immune function was further evaluated by analyzing the changes in spleen index, thymus index, and the ratio of peripheral blood granulocytes, monocytes, and lymphocytes. Meanwhile, the proportion of NCR⁺ group 3 innate lymphoid cells (ILC3), NCR⁻ILC3, and IL-22⁺ILC3 in colonic lamina propria lymphocytes of mice was detected by flow cytometry. The contents of effectors IL-22, IL-17A, and GM-CSF were detected by RT-PCR. We use cell scratching to determine the effect of DMD conditioned medium on the migration of Caco-2 cells by establishing an in vitro model of MNK-3 conditioned medium (CM) intervening Caco-2 cells. RT-PCR and WB detect the expression of tight junction ZO-1, Occludin, and Claudin-1. DMD restores the body weight, colon length, peripheral blood RBC numbers, and HGB content of chronic colitis mice and reduces peripheral blood WBC and colon inflammatory cell infiltration. Moreover, DMD decreased LPS content in serum, bacterial infiltration of colonic mucosa, and bacterial translocation in spleen and mesenteric lymph nodes. Simultaneously, DMD intensifies the expression of ZO-1, Occludin, and Claudin-1, the ratio of NCR⁺ILC3 and IL-22⁺ILC3, and decreases the proportion of NCR⁻ILC3. In vitro studies also confirm that the conditioned medium of DMD promotes the migration of Caco-2 cells and the expression of tight junction proteins. Our results confirm that DMD improves inflammation and restores intestinal epithelial function in mice with chronic colitis, and the mechanism may be related to regulating ILC3 function.
Keywords	bacterial culture ; blood serum ; body weight ; colon ; flow cytometry ; fluorescence ; granulocytes ; hemoglobin ; immune response ; inflammation ; interleukin-17 ; intestinal mucosa ; lymph ; mice ; models ; monocytes ; nucleic acid hybridization ; occludins ; spleen ; therapeutics ; tight junctions ; traditional medicine ; ulcerative colitis
Language	English
Dates of publication	2022-0816
Publishing place	Elsevier B.V.
Document type	Article
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.2022.115652
Database	NAL-Catalogue (AGRICOLA)

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