Font Size: a A A

Mechanism Of Dioscin Improves Postmenopausal Osteoporosis

Posted on:2020-02-10Degree:MasterType:Thesis
Country:ChinaCandidate:J ZhaoFull Text:PDF
GTID:2404330572477944Subject:Obstetrics and gynecology
Abstract/Summary:PDF Full Text Request
Purpose:To investigate the effects of dioscin against PMO in an osteoporotic ovariectomized rat model,as well as on a cultured osteoblast precursor cell line and propose the possible molecular mechanisms of action,to further verify the feasibility of clinical application of dioscin.Methods:We successfully established PMO rat models by ovariectomy.Western blot was used to explore the expression of proteins including PI3K,P38,ERK,AKT,Bcl-2,Bax and c-Caspase3 in the bone tissue.Besides,MC3T3-E1 cells were cultured in rats' serum,the cell counting and MTT assay of which were performed.Results:1.Dioscin increased the bone mineral density(BMD)and enhanced the bone mechanical properties of PMO rats in low(P<0.05)and high(P<0.01)dose groups.Dioscin increased bone trabeculae formation of bones in PMO rats.2.Dioscin promoted the ALP and BMP expression.3.The expression of PI3K/P38/p-ERK in low dose group was increased(P<0.01),and the expression of PI3K/P38/p-AKT in high dose group was increased.(P<0.01).4.In low dose group,the expression of Bcl-2 was increased(P<0.01),and the expression of c-Caspase3 was decreased(P<0.05).In high dose group,the expression of Bcl-2 was increased(P<0.01),and the expression of Bax and c-Caspase3 was decreased(P<0.05).5.Dioscin enhanced the proliferation of MC3T3-E1 cells.Conclusions:1.Dioscin increased the bone mineral density(BMD)of PMO rats and enhanced the bone mechanical properties of PMO rats.2.Dioscin promoted bone formation via PI3K/P38/AKT signaling pathway.3.Dioscin inhibited the apoptosis of bone tissue via Bcl-2/Bax signaling pathway.
Keywords/Search Tags:dioscin, postmenopausal osteoporosis, PI3K/P38/AKT pathway, apoptosis, MC3T3-E1 cell
PDF Full Text Request
Related items