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Compound Flaxi

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Naringin has been shown to be cartilageprotective by decreasing the expression of these inflammatory cytokines, reactive oxygen species, and destructive enzymes.Osteomyelitis is characterized by the proliferation of bacteria that degrade bone both directly via bacterial products and indirectly by inducing inflammation productive of osteoclastic cytokines.A combined day regimen of oral naringin and treadmill exercise in OVX mice more effectively reduced the structural effects of osteoporosis on bone mass and increased bone strength than either monotherapy.Importantly, naringin administration in OVX mice has not been associated with increases in uterus weight, suggesting that the offtarget estrogenmodulating effects of estrogen are limited.This represents a significant advantage over traditional postmenopausal hormone replacement therapy, which nonselectively acts upon bone, breast, ovarian, and endometrial tissue.Perhaps the greatest therapeutic benefit of naringin in the treatment of osteoporosis has been demonstrated in models of disuseinduced osteoporosis.These conditions replicate the loss of bone mechanical loading seen in limited mobility and bedridden patients and astronauts in zerogravity environments.Dosedependent recovery of trabecular microarchitecture and bone formation rates comparable to the sham group were observed with naringin treatment.Several theories have been postulated regarding the etiology of naringins bonepreserving effects in osteoporosis in in vivo models.Naringin is believed to limit the upregulation of osteoclast activity and differentiation seen in osteoporosis.In addition to mediating osteoclastogenesis, naringin has the potential to induce new bone formation in osteoporotic animals by upregulating the differentiation and activity of osteoblasts, as described previously.Finally, naringin may also prevent microvascular damage to osteopenic and osteoporotic bone.Naringin preserves bone microvascularity in OVX mice and reduces the perturbations of NO and endothelin levels, two key regulators of vasoactivity, seen in osteoporosis.In addition, naringin promotes angiogenesis and neovascularization during fracture callus formation in murine osteoporotic models, likely by way of vascular endothelial growth factor expression changes in osteocytes.These effects resulted in the dosedependent acceleration of fracture healing in murine models.More work is needed to further elucidate the mechanisms by which naringin exerts its effects upon bone resident cells in osteoporosis.Pharmacological therapy for osteoporosis targets both osteoclastogenesis and new bone formation with agents such as bisphosphonates and intermittent parathyroid hormone, respectively.However, the reduced responsivity of protracted disuse osteoporosis to bisphosphonate treatment and transition from bone formation to adipogenesis in bone marrow with age necessitate the adoption of new osteostimulative and osteoprotective therapies.On the cellular level, these processes increase osteoclastogenesis and reduce osteoblast levels and activity.Consequently, diabetic rats display reduced trabecular volume and bone remodeling and formation, with increased trabecular spacing in the femur and lumbar spine, similar to the findings clinically observed in various forms of osteoporosis. In vivo models of Targetmol's CORM3,132 diabetes typically utilize streptozocin injections, which damage the cells of the pancreas, to recreate the pathology seen in type DM or prolonged feeding of high fat diets to simulate type DM.Increased levels of superoxide dismutase activity in bone marrow are indicative of higher levels of inflammation and oxidative stress, which have been implicated in the pathogenesis of diabetes.Naringin has been found to normalize both SOD and CAT levels in diabetic rats.Naringin administration to diabetic rodents resulted in similar oxidative stress attenuation in the skin, liver, pancreas, and kidney.

asked Apr 7 in Asiaworld by anonymous

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