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Study On The Protective Effect And Mechanism Of Different Concentrations Of Icariin On Iron Overload Injury Of Osteoblasts

Posted on:2018-03-24Degree:MasterType:Thesis
Country:ChinaCandidate:S L WuFull Text:PDF
GTID:2334330566451823Subject:Surgery (orthopedics)
Abstract/Summary:PDF Full Text Request
OBJECTIVE With China’s aging population,postmenopausal women with osteoporosis is increasing,iron overload as a new risk factors involved in the pathogenesis of osteoporosis,through the study of protective effect and mechanism of different concentrations of Icariln on bone cell iron overload damage,provide a new method for the treatment of women postmenopausal osteoporosis.METHODS The experiment was divided into 3 groups,normal group,iron overload group(FAC),Iron overload +ICA intervention group(FAC+ Low,medium and high dose ICA)Cells in each group intervention treatment for 96 h,CCK-8 assay was used to detect the cell proliferation activity,flow cytometry was used to detected cell apoptosis and necrosis,reactive oxygen species,mitochondrial membrane potential;western blot was used to detect the expression of oxidases(NADPH oxidases 4(NOX4)in each group.RESULTS Compared with normal group,the proliferative activity of osteoblasts was significantly lower than that of normal group.The expression of NOX4 in cells increased significant ly,the ROS increased and the mitochondrial membrane potential decreased significantly.ICA intervention group compared with iron overload group,Osteoblast proliferation activity increased significantly,the level of apoptosis decreased,expression of NOX4 and ROS production in cells decreased,mitochondrial membrane potential in osteoblasts increased.CONCLUSION ICA has protective effects on the injury of osteoblasts induced by iron overload,Its specific protective mechanism may be related to its inhibition of NOX4 mediated ROS production,protection of mitochondria,thereby inhibiting intracellular apoptosis...
Keywords/Search Tags:Osteoporosis, osteoblast, icariin, iron overload, oxidative stress, mitochondrial apoptosis pathway, cell death
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