epimedin-c has been researched along with Disease-Models--Animal* in 3 studies
3 other study(ies) available for epimedin-c and Disease-Models--Animal
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Epimedin C modulates the balance between Th9 cells and Treg cells through negative regulation of noncanonical NF-κB pathway and MAPKs activation to inhibit airway inflammation in the ovalbumin-induced murine asthma model.
Topics: Animals; Asthma; Bronchoalveolar Lavage Fluid; Cytokines; Disease Models, Animal; Female; Flavonoids; Inflammation; Lung; Mice; Mice, Inbred BALB C; Ovalbumin; T-Lymphocytes, Helper-Inducer; T-Lymphocytes, Regulatory | 2020 |
Epimedin C Promotes Vascularization during BMP2-Induced Osteogenesis and Tumor-Associated Angiogenesis.
Epimedin C is one of the chemical markers and major flavonoids in Herba Epimedii (Yinyanghuo), which is traditionally used to treat bone diseases and gonadal dysfunction in China. Our previous study indicated that epimedin C could induce endothelial-like, but not osteogenic differentiation of C3H/10T1/2 cells in vitro. As vasculogenesis plays a pivotal role in bone formation, this study used the bone morphogenetic protein 2 (BMP2) induced ectopic bone formation model and mice 4T1 breast cancer cells co-implanted with luciferase labeled C3H/10T1/2 cells (4T1 [Formula: see text] C3H/10T1/2-Luc) model to examine the in vivo effects of Epimedin C on vasculogenesis. As a result, Epimedin C significantly increased the bone weight and blood perfusion of mice in the BMP2 induced ectopic osteogenesis model, and the bone in Epimedin C [Formula: see text] BMP2 group was more mature than that in BMP2 group. In addition, the tumor weight, blood perfusion and tumor-associated angiogenesis were also significantly increased in the Epimedin C treated 4T1 tumor bearing mice. The mRNA levels of endothelial markers, such as the platelet endothelial adhesive factor-1(CD31), the endothelial cell specific molecule-1(ESM-1), and the vascular von Willebrand factor (vWF) in mouse 4T1 mammary tumor tissue, were commonly found to occur alongside the luciferase (labeled in C3H/10T1/2 cells) expression and significantly increased after Epimedin C treatment. Taken together, Epimedin C can effectively promote vascularization both in the BMP2-depended bone formation model and in the 4T1 mammary tumor-bearing model by inducing an endothelial-like differentiation of C3H/10T1/2 in BALB/c nude mice. Topics: Animals; Bone Morphogenetic Protein 2; Cell Differentiation; Cell Line; Cell Line, Tumor; Cells, Cultured; Disease Models, Animal; Drugs, Chinese Herbal; Endothelial Cells; Female; Flavonoids; Mammary Neoplasms, Experimental; Mice, Inbred BALB C; Mice, Nude; Neovascularization, Pathologic; Ossification, Heterotopic; Osteogenesis; Phytotherapy | 2017 |
[Activity Study of Icarlin and Epimedin C Monomer under the Same Molarity in Osteoporosis Ze- brafish Model].
Objective To evaluate anti-osteoporotic activity of icariin and Epimedin C monomer under the same molarity in predinsolone-induced osteoporosis zebrafish. Methods Zebrafish larvae after 4-day fertilization were divided into group S [0. 5% dimethyl sulfoxide (DMSO) , A (25 μmol/L prednisolone, 0. 5% DMSO), B (2 IU/L salmon calcitonin, 25 μmol/L prednisolone,0. 5% DMSO), C (1. 5 1,mol/L icariin, 25 μmol/L prednisolone, 0. 5% DMSO) , D (15 μLmol/L icariin,25 μmol/L prednisolone, 0. 5% DM- SO), E (150 μmol/L icariin, 25 μmol/L prednisolone, 0. 5% DMSO), F (1. 5 μmol/L Epimediri C, 25 μmol/L prednisolone, 0. 5% DMSO) , G (15 μmol/L Epimedin C, 25 μmol/L prednisolone, 0.5% DM- SO) , H (150 μmol/L Epimedin C, 25 μmol/L prednisolone, 0. 5% DMSO). All culture solution contained 0. 5% DMSO. All the young fishes were grown in a 24-well plate. The culture medium was changed every day. They were cultured in a incubator box at 28. 5 °C and killed at day 9. Zebrafish skeleton was stained with alizarin red. The stained Zebrafish ventral skull was observed using microscope, and mineralized area was quantitatively analyzed. Results Compared with group S, accumulative integrated optical densi- ty(IOD)of the mineralized area significantly decreased in group A (P <0. 01) ; accumulative IOD of the mineralized area significantly increased in group B (P <0. 01). The accumulative IOD of the mineralized area showed weakly increasing tendency in group C, D, and E along with increased concentration (P < 0. 05). Compared with group A, accumulative IOD obviously increased in group B with statistical difference (P <0. 01) , but with no statistical difference as compared with group C or group D (P >0. 05). Statistical difference existed in accumulative IOD between group A and group E (P <0. 05). The mineralized area showed increasing tendency in group F and group G along with increased concentration (P <0. 05), and accumulative IOD obviously increased as well (P <0. 05). No Zebrafish embryo survived in group H. There was no statistical difference in Zebrafish embryo survival among group E, F, or G (P >0. 05). The staining of Zebrafish skull was clearly seen in group S, with vertebrae and bilateral branchial skeleton clearly seen. The intensity of staining in the same area was obviously attenuated in group A. The osteo- genesis was speeded up under the same condition in group B, with obviously enlarged mineralized area and more darkly stained bone tissue. The mineralization of skull was Topics: Animals; Disease Models, Animal; Flavonoids; Glucosides; Osteoporosis; Zebrafish | 2016 |