icariin/hypoxia

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Icariin increases chondrocyte vitality by promoting hypoxia-inducible factor-1α expression and anaerobic glycolysis.

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Articular cartilage is a unique avascular tissue in which chondrocytes are embedded in extracellular matrix (ECM). The decreased ECM resulting from the loss of articular chondrocyte viability leads to degenerative diseases such as osteoarthritis (OA). This study aims to investigate the

[Effect of icariin on hypoxia/reoxygenation injury in neonatal rat cardiomyocytes].

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OBJECTIVE To investigate the effect of icariin on myocardial hypoxia reoxygenation injury and the possible mechanism. METHODS Neonatal Sprague-Dawley rat cardiomyocytes in primary culture were treated with different concentrations of icariin for 24 h prior to hypoxia/reoxygenation injury.

Icariin alleviates hypoxia-induced damage in MC3T3-E1 cells by down-regulating TALNEC2.

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Osteonecrosis is a harmful musculoskeletal disease. We aims to detect the effects of Icariin (ICA) in MC3T3-E1 cell.MC3T3-E1 cell was pretreated with ICA and was subjected to hypoxia stimuli. The TALNEC2 overexpression or silencing vectors (pTALNEC2 or

[Effect of icariin on hypoxia induced vascular endothelial cells injury].

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OBJECTIVE To study the effect of icariin on vascular endothelial cells (VECs) injury induced by hypoxia. METHODS The hypoxia-ischemia model was established. The effect of icariin on injury of VECs activity induced by hypoxia was determined by MTT assay. The levels of malondialdehyde (MDA),

Icariin attenuates hypoxia-induced oxidative stress and apoptosis in osteoblasts and preserves their osteogenic differentiation potential in vitro.

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OBJECTIVE Icariin, a prenylated flavonol glycoside isolated from traditional Chinese medicinal herb of the genus Epimedium, has been demonstrated to be a potential alternative therapy for osteoporosis, and its action mechanism so far has been mainly attributed to its phytoestrogenic property. As

Flavonoid Compound Icariin Activates Hypoxia Inducible Factor-1α in Chondrocytes and Promotes Articular Cartilage Repair.

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Articular cartilage has poor capability for repair following trauma or degenerative pathology due to avascular property, low cell density and migratory ability. Discovery of novel therapeutic approaches for articular cartilage repair remains a significant clinical need. Hypoxia is a hallmark for

Neuroprotective effects of icariin in neonatal hypoxia-ischemic brain damage via its anti-apoptotic property

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Introduction: Neonatal hypoxic-ischemic brain damage (HIBD) is a brain disease that is caused by perinatal asphyxia. Icariin (ICA), which is an active component of Epimedii (a Chinese medicinal herb), has been verified to demonstrate a

Icariin protects against intestinal ischemia-reperfusion injury.

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BACKGROUND This study investigated the role of Sirtuin 1 (SIRT1)/forkhead box O3 (FOXO3) pathway, and a possible protective function for Icariin (ICA), in intestinal ischemia-reperfusion (I/R) injury and hypoxia-reoxygenation (H/R) injury. METHODS Male Sprague-Dawley rats were pretreated with

Screening of anti-hypoxia/reoxygenation agents by an in vitro model. Part 1: Natural inhibitors for protein tyrosine kinase activated by hypoxia/reoxygenation in cultured human umbilical vein endothelial cells.

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Protein tyrosine kinase (PTK) signaling pathways play important roles in ischemia/reperfusion (I/R) or hypoxia/reoxygenation (H/R) injuries. Inhibition of PTK activation can protect against I/R- or H/R-induced damages. As one part of our work for seeking bioactive compounds from natural sources

[Effects of icariin on the erectile function and expression of nitrogen oxide synthase isoforms in corpus cavernosum of arterigenic erectile dysfunction rat model].

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OBJECTIVE The study the effects of oral administered icariin on intracavernosal pressure (ICP) and on expression of the nitrogen oxide synthase (NOS) isoforms in corpus cavernosum (CC) of arteriogenic erectile dysfunction (A-ED) rat model. METHODS Forty adult male Wistar rats were randomly divided

Icariin promotes the migration of bone marrow stromal cells via the SDF-1α/HIF-1α/CXCR4 pathway.

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In this study, a series of in vitro experiments were performed to investigate the molecular mechanisms underlying cell migration promoted by icariin (ICA) at low concentrations.Bone marrow stromal cells (BMSCs) were cultured with different concentrations of

Screening of anti-hypoxia/reoxygenation agents by an in vitro method. Part 2: Inhibition of tyrosine kinase activation prevented hypoxia/reoxygenation-induced injury in endothelial gap junctional intercellular communication.

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In this study, we demonstrated that hypoxia/reoxygenation (H/R) induced an injury in gap junctional intercellular communication (GJIC) after 2 h of reoxygenation in cultured HUVEC. Free radical scavenger (DMSO) and antioxidant (SOD) did not prevent this GJIC injury at all. Protein kinase C inhibitor

Icariin inhibits osteoclast differentiation and bone resorption by suppression of MAPKs/NF-κB regulated HIF-1α and PGE(2) synthesis.

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Icariin has been reported to enhance bone healing and treat osteoporosis. In this study, we examined the detail molecular mechanisms of icariin on lipopolysaccharide (LPS)-induced osteolysis. Our hypothesis is that icariin can inhibit osteoclast differentiation and bone resorption by suppressing

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