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作 者:赵玉芹[1] 张成杰[1] 相淑芳[2] ZHAO Yuqin;ZHANG Chengjie;XIANG Shufang(Department of Emergency,Binzhou People's Hospital,Binzhou 256610,P.R.China;Department of Obstetrics,Binzhou People's Hospital)
机构地区:[1]滨州市人民医院急诊科,滨州256610 [2]滨州市人民医院产科
出 处:《滨州医学院学报》2019年第4期291-294,共4页Journal of Binzhou Medical University
摘 要:目的探讨熊果酸衍生物(ursolic acid derivatives,UAD)对糖尿病骨质疏松骨重塑的影响。方法将小鼠随机分为对照组、STZ组与US组三组,取胫骨进行基因和蛋白表达测定以及组织形态学分析,测定骨体积/总体积(BV/TV)、骨小梁数(Tb.N)、小梁厚度(Tb.Th)和骨密度/总体积(BMD/TV)等各项骨形态参数,分别检测骨保护素/核因子-κΒ受体活化剂(OPG/RANKL)比值与骨代谢关键调控因子mRNA的表达。结果STZ组与对照组相比,OPG/RANKL比值和OPG显著降低且RANKL升高;US组显著增加OPG/RANKL比值。STZ组MMP9和CAII mRNA表达显著高于对照组,而STZ组Runx2和TGF-β的mRNA表达显著低于对照组。US组同时逆转糖尿病小鼠MMP9、CAII、RUNX2和TGF-βmRNA的表达。结论UAD通过促进成骨细胞分化、新生骨形成及抑制破骨细胞骨吸收功能来逆转STZ诱导的骨小梁损伤作用进行骨重塑。Objective The aim of this study was to investigate the effects of ursolic acid derivatives(UAD)on bone remodeling in diabetic osteoporosis.Methods The mice were randomly divided into three groups:control group,STZ group and US group.The tibia was taken for gene and protein expression determination and histomorphologicalanalysis.Bone volume/total volume(BV/TV),trabecular number(Tb.N),trabecular thickness(Tb.Th)and bone mineral density/total volume(BMD/TV)were measured.Detection of osteoprotegerin/nuclear factor-kappa B receptor activator(OPG/RANKL)ratio and expression of key regulators of bone metabolism.Results Compared with the control group,OPG/RANKL ratio and OPG in STZ group decreased significantly and RANKL increased significantly.The OPG/RANKL ratio increased significantly in US group.The expression of MMP9 and CAI in STZ group was significantly higher than that in control group,while the expression of Runx2 and TGF-beta in STZ group was significantly lower than that in control group.US group reversed the expression of MMP9,CAII,RUNX2 and TGF-beta in diabetic mice at the same time.Conclusion UAD reverses STZ-induced trabecular bone injury by promoting osteoblast differentiation,new bone formation and inhibiting osteoclast bone resorption.
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