bay-11-7082 and Calcinosis

bay-11-7082 has been researched along with Calcinosis* in 1 studies

Other Studies

1 other study(ies) available for bay-11-7082 and Calcinosis

Article	Year
Lazaroid U-74389G inhibits the osteoblastic differentiation of IL-1β-indcued aortic valve interstitial cells through glucocorticoid receptor and inhibition of NF-κB pathway. The Journal of steroid biochemistry and molecular biology, 2015, Volume: 152 Aortic valve calcification is characterized as the active process of aortic valve interstitial cells (AVICs), and considered as an inflammatory disease. As an antioxidant, the anti-inflammatory activity of Lazaroid has been exhibited in various models. We hypothesized that Lazaroid U-74389G would inhibit the osteoblastic differentiation of AVICs induced by IL-1β.. Normal tricuspid aortic valve leaflets were collected from patients with acute aortic dissection (Type A) undergoing the Bentall procedure. AVICs were isolated and stimulated with IL-1β in presence or absence of U-74389G in culture. Cell lysates were analyzed for osteogenic markers and nuclear factor-κB using real-time PCR and Immunoblotting. Culture media was analyzed for IL-6 and IL-8 with enzyme-linked immunosorbent assay. Alizarin Red Staining was adopted to demonstrate the calcium deposition.. The expression of alkaline phosphatase and bone morphogenetic protein, accompanied by the production of IL-6 and IL-8, was up-regulated in response to IL-1β and was inhibited by the addition of U-74389G. The NF-κB pathway was activated by IL-1β and involved in the suppression of U-74389G on osteoblastic differentiation in AVICs. The negative effects of U-74389G on ostengenic gene expression and mineralization of AVICs were blocked by glucocorticoid receptor antagonist mifepristone and the NF-κB inhibitor Bay 11-7082.. U-74389G inhibits the pro-osteogenic response to IL-1β stimulation in AVICs. The osteoblastic differentiation and mineralization of AVICs were inhabited by U-74389G though the modulation of NF-κB activation, and this pathway could be potential therapeutic targets for medical treatment of calcified aortic valve disease. Topics: Alkaline Phosphatase; Aortic Valve; Aortic Valve Stenosis; Bone Morphogenetic Proteins; Calcinosis; Cell Differentiation; Cells, Cultured; Humans; Inflammation Mediators; Interleukin-1beta; Interleukin-6; Interleukin-8; Male; Mifepristone; Myocytes, Smooth Muscle; Nitriles; Osteoblasts; Osteogenesis; Phosphorylation; Pregnatrienes; Receptors, Glucocorticoid; Sulfones; Transcription Factor RelA; Tricuspid Valve	2015

Article

Year

Lazaroid U-74389G inhibits the osteoblastic differentiation of IL-1β-indcued aortic valve interstitial cells through glucocorticoid receptor and inhibition of NF-κB pathway.

The Journal of steroid biochemistry and molecular biology, 2015, Volume: 152

Aortic valve calcification is characterized as the active process of aortic valve interstitial cells (AVICs), and considered as an inflammatory disease. As an antioxidant, the anti-inflammatory activity of Lazaroid has been exhibited in various models. We hypothesized that Lazaroid U-74389G would inhibit the osteoblastic differentiation of AVICs induced by IL-1β.. Normal tricuspid aortic valve leaflets were collected from patients with acute aortic dissection (Type A) undergoing the Bentall procedure. AVICs were isolated and stimulated with IL-1β in presence or absence of U-74389G in culture. Cell lysates were analyzed for osteogenic markers and nuclear factor-κB using real-time PCR and Immunoblotting. Culture media was analyzed for IL-6 and IL-8 with enzyme-linked immunosorbent assay. Alizarin Red Staining was adopted to demonstrate the calcium deposition.. The expression of alkaline phosphatase and bone morphogenetic protein, accompanied by the production of IL-6 and IL-8, was up-regulated in response to IL-1β and was inhibited by the addition of U-74389G. The NF-κB pathway was activated by IL-1β and involved in the suppression of U-74389G on osteoblastic differentiation in AVICs. The negative effects of U-74389G on ostengenic gene expression and mineralization of AVICs were blocked by glucocorticoid receptor antagonist mifepristone and the NF-κB inhibitor Bay 11-7082.. U-74389G inhibits the pro-osteogenic response to IL-1β stimulation in AVICs. The osteoblastic differentiation and mineralization of AVICs were inhabited by U-74389G though the modulation of NF-κB activation, and this pathway could be potential therapeutic targets for medical treatment of calcified aortic valve disease.

Topics: Alkaline Phosphatase; Aortic Valve; Aortic Valve Stenosis; Bone Morphogenetic Proteins; Calcinosis; Cell Differentiation; Cells, Cultured; Humans; Inflammation Mediators; Interleukin-1beta; Interleukin-6; Interleukin-8; Male; Mifepristone; Myocytes, Smooth Muscle; Nitriles; Osteoblasts; Osteogenesis; Phosphorylation; Pregnatrienes; Receptors, Glucocorticoid; Sulfones; Transcription Factor RelA; Tricuspid Valve

2015