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10.1177/1535370217701005 http://scihub22266oqcxt.onion/10.1177/1535370217701005 C5407594!5407594 !28440736     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=28440736 &cmd=llinks): Failed to open stream: HTTP request failed! 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Levistilide A inhibits angiogenesis in liver fibrosis via vascular endothelial growth factor signaling pathway |pdf=|usr=}}{{28440736 }} gab.com Text Levistilide A inhibits angiogenesis in liver fibrosis via vascular endothelial growth factor signaling pathway JO: Exp Biol Med (Maywood) http://www.kidney.de/pget.php?&tw=1&pmid=28440736 #FOAvip Levistilide A (C(24)H(28)O(4), molecular weight?=?380.48) derived from Angelica sinensis (Danggui) has been reported to inhibit hepatic stellate cell proliferation. This study investigated the effects of levistilide A on liver fibrosis relating to angiogenesis, particularly on the characteristic change in liver sinusoidal endothelial cells. LX-2 cells were activated by TGF-?1, and the human hepatic sinusoidal endothelial cells (HHSECs) were induced by endothelial cell growth supplement. Cell viability was detected using a methylthiazoldiphenyl-tetrazolium bromide assay; F-actin was visualized through the fluorescence probe method; cell proliferation was examined using the EdU kit; antiangiogenesis activity was assessed using the tube formation assay and transgenic zebrafish model. To verify the results in vivo, rats were subcutaneously injected with CCl(4) twice a week for six weeks to duplicate the liver fibrosis model and then treated with 10?mL/kg of normal saline, 4?mg/kg of sorafenib, and 3 and 6?mg/kg of levistilide A for three weeks from the fourth week. Collagen deposition was detected through Sirius Red staining; liver microvasculature was examined through vWF labeling and X-ray 2D imaging; sinusoidal fenestrations were observed through scanning electron microscopy; collagen I, ?-SMA, CD31, vascular endothelial growth factor (VEGF), and VEGF-R2 were detected through Western blotting. Our results indicated that levistilide A attenuated LX-2 cell activation and HHSEC proliferation. The ability of HHSECs to form tubelike structures in Matrigel was inhibited, and the number of functional vessels in transgenic zebrafish decreased. In in vivo experiments, levistilide A reduced collagen deposition and the number of new microvessels; ameliorated sinusoid capillarization; and downregulated the expression of CD31, VEGF, and VEGF-R2. These findings suggest that levistilide A can inhibit liver fibrosis through antiangiogenesis by alleviating sinusoid capillarization via the VEGF signaling pathway. Impact statement Levistilide A has been reported to inhibit hepatic stellate cell (HSC) proliferation. In this study, we further investigated the mechanisms of levistilide A on liver fibrosis relating to angiogenesis, particularly on the characteristic change in liver sinusoidal endothelial cells. The cell models of HSC and liver sinusoidal endothelial cell and CCl(4) induced liver fibrosis model were used. These results suggest that levistilide A can inhibit liver fibrosis through antiangiogenesis by alleviating sinusoid capillarization via the vascular endothelial growth factor signaling pathway. The effect of levistilide A on liver fibrosis was confirmed, and its detailed mechanism was also discussed. These findings suggest that levistilide A may be a great potential drug for treating liver fibrosis through antiangiogenesis, and this effect will be verified in other fibrotic animal model studies or by clinical trials. Twit Text FOAVip Levistilide A inhibits angiogenesis in liver fibrosis via vascular endothelial growth factor signaling pathway ????Exp Biol Med (Maywood) http://www.kidney.de/pget.php?&tw=1&pmid=28440736 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28440736 #FOAvip English Wikipedia <ref>{{Cite pmid|28440736 }}</ref> Levistilide A inhibits angiogenesis in liver fibrosis via vascular endothelial growth factor signaling pathway #MMPMID28440736 Zhao ZM ; Liu HL ; Sun X ; Guo T ; Shen L ; Tao YY ; Liu CH Exp Biol Med (Maywood) 2017[May]; 242 (9 ): 974-985 PMID28440736 show ga Levistilide A (C(24)H(28)O(4), molecular weight?=?380.48) derived from Angelica sinensis (Danggui) has been reported to inhibit hepatic stellate cell proliferation. This study investigated the effects of levistilide A on liver fibrosis relating to angiogenesis, particularly on the characteristic change in liver sinusoidal endothelial cells. LX-2 cells were activated by TGF-?1, and the human hepatic sinusoidal endothelial cells (HHSECs) were induced by endothelial cell growth supplement. Cell viability was detected using a methylthiazoldiphenyl-tetrazolium bromide assay; F-actin was visualized through the fluorescence probe method; cell proliferation was examined using the EdU kit; antiangiogenesis activity was assessed using the tube formation assay and transgenic zebrafish model. To verify the results in vivo, rats were subcutaneously injected with CCl(4) twice a week for six weeks to duplicate the liver fibrosis model and then treated with 10?mL/kg of normal saline, 4?mg/kg of sorafenib, and 3 and 6?mg/kg of levistilide A for three weeks from the fourth week. Collagen deposition was detected through Sirius Red staining; liver microvasculature was examined through vWF labeling and X-ray 2D imaging; sinusoidal fenestrations were observed through scanning electron microscopy; collagen I, ?-SMA, CD31, vascular endothelial growth factor (VEGF), and VEGF-R2 were detected through Western blotting. Our results indicated that levistilide A attenuated LX-2 cell activation and HHSEC proliferation. The ability of HHSECs to form tubelike structures in Matrigel was inhibited, and the number of functional vessels in transgenic zebrafish decreased. In in vivo experiments, levistilide A reduced collagen deposition and the number of new microvessels; ameliorated sinusoid capillarization; and downregulated the expression of CD31, VEGF, and VEGF-R2. These findings suggest that levistilide A can inhibit liver fibrosis through antiangiogenesis by alleviating sinusoid capillarization via the VEGF signaling pathway. Impact statement Levistilide A has been reported to inhibit hepatic stellate cell (HSC) proliferation. In this study, we further investigated the mechanisms of levistilide A on liver fibrosis relating to angiogenesis, particularly on the characteristic change in liver sinusoidal endothelial cells. The cell models of HSC and liver sinusoidal endothelial cell and CCl(4) induced liver fibrosis model were used. These results suggest that levistilide A can inhibit liver fibrosis through antiangiogenesis by alleviating sinusoid capillarization via the vascular endothelial growth factor signaling pathway. The effect of levistilide A on liver fibrosis was confirmed, and its detailed mechanism was also discussed. These findings suggest that levistilide A may be a great potential drug for treating liver fibrosis through antiangiogenesis, and this effect will be verified in other fibrotic animal model studies or by clinical trials. |Animals [MESH] |Disease Models, Animal [MESH] |Gastrointestinal Agents/*administration & dosage [MESH] |Heterocyclic Compounds, Bridged-Ring/*administration & dosage [MESH] |Liver Cirrhosis/chemically induced/*drug therapy/*pathology [MESH] |Liver/pathology [MESH] |Neovascularization, Pathologic/*pathology [MESH] |Niacinamide/administration & dosage/analogs & derivatives [MESH] |Phenylurea Compounds/administration & dosage [MESH] |Rats [MESH] |Sorafenib [MESH] |Treatment Outcome [MESH]Levistilide A inhibits angiogenesis in liver fibrosis via vascular end(epmc).pdf DeepDyve Pubget Overpricing