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These effects are postulated to stem from the positive regulation of glucose metabolism and GLUT mobilization by naringin.In addition, the effects of naringin upon serum lipid regulation have been extensively investigated in vivo.The favorable lipid regulatory profile of naringin may be linked to its positive effects on bone secondary to its promotion of vascular and microvascular health.The relationship between hyperlipidemia and diabetic microangiopathy, resulting in reduced vascular delivery to bone and local hypoxia, inflammation, and oxidative stress responses, is well established.Naringin administration reduces the sell 4-Hydroxytamoxifen expression of various serum markers of inflammation in in vivo models of DM.The aortae of diabetic mice treated with naringin displayed less endothelial damage, as visualized on transmission electron microscopy, as well as greater vascular functionality, as measured by responsivity to exogenously administered epinephrine, acetylcholine, and insulin.Moreover, naringin has been observed to induce SEMA, a local bone microenvironmental factor that both promotes new bone formation and reduces bone resorption, expression in vivo.Although these medications are effective in their ability to suppress the immune system, their deleterious effects are many, particularly upon bone.Chronic exogenous steroid administration contributes to osteopenia, osteoporosis, pathologic fracture, poor fracture healing, and avascular necrosis.In vivo models of glucocorticoidtreated mice have demonstrated that glucocorticoids not only reduce trabecular bone volume and whole bone strength, but also alter the osteocyte lacunae microenvironment, thereby decreasing the bone mineral to matrix ratio and increasing bone fragility. In this way, high dose andor chronic glucocorticoid administration begets osteopenia and osteoporosis.In a rabbit model of steroidinduced avascular necrosis of the femoral head, naringin treatment significantly mitigated steroidassociated reductions in serum OCN levels and observed rates of osteonecrosis.Multiple signaling pathways have been implicated in the pathogenesis of glucocorticoidinduced osteoporosis expression have been observed in osteoporotic mice.GIO rats demonstrated decreased expression of BMP and RUNX, thus impairing osteoblastic differentiation.Phosphoinositide kinase are also disrupted in GIO, resulting in perturbed bone growth and formation.Naringin therapy was associated with lower total cholesterol levels and lowdensity lipoproteinhighdensity lipoprotein ratios in SANFH animals.The modulation of these signaling pathways in bone by naringin, as detailed previously, are indicative of naringins manifold local and systemic inflammatory effects.Additional in vivo research of the effects of naringin in models of GIO, fracture healing, and avascular necrosis are needed to more effectively prevent and combat glucocorticoidinduced conditions of bone.In a mouse model of ankylosis spondylitis, intraperitoneal flavonoid therapy reduced the expression of TNF, IL, IL, signal transducer and activator of transcription in a dosedependent fashion.These effects on estrogen receptors have been described extensively with respect to osteoporosis both in vitro and in vivo but require further elucidation in the setting of osteoarthritis.The spread of infection from bone to surrounding soft tissue reduces vascular supply to bone, allowing for the formation of a sequestrum, or area of dead bone, constraining the medullary and periosteal blood supplies.Given the persistence, recurrence, and severe morbidity and mortality of osteomyelitis despite antibiotic treatment, new and improved therapeutic options are being sought.Though the flavonones promote bone health by reducing inflammatory injury and osteolysis and increasing new bone formation, their effects in osteomyelitis have yet to be thoroughly characterized.

asked Apr 6 in SYDT by anonymous

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