摘要
[目的]探究花椒素WGX-50调控OPG/RANK/RANKL通路对骨质疏松小鼠的影响。[方法]将C57BL/6小鼠随机分为5组:对照组、骨质疏松组、WGX-50低剂量组、WGX-50中剂量组、WGX-50高剂量组。连续21 d、1次/d灌胃小鼠维甲酸(90 mg/kg),建立骨质疏松模型。WGX-50低、中、高剂量组小鼠每日分别灌胃0.5、1、2 mg/kg WGX-50,连续28 d。对照组、骨质疏松组小鼠灌胃生理盐水。完成末次给药24 h后,以骨密度仪检测各组小鼠骨密度,比色法分析小鼠血清的骨代谢指标(钙、磷)水平,酶联免疫吸附测定实验检测小鼠血清骨生成指标(碱性磷酸酯酶、骨钙素)水平,苏木素-伊红染色分析小鼠股骨组织的病理变化,Western blot分析小鼠股骨组织OPG、RANK、RANKL蛋白的表达。[结果]与骨质疏松组小鼠相比,WGX-50低、中、高剂量组小鼠的股骨损伤减轻、骨密度增加(P<0.05)、骨生成指标(碱性磷酸酶与骨钙素)水平升高(P<0.05)、骨代谢指标(钙与磷)水平降低(P<0.05)、OPG蛋白表达增加、RANK与RANKL蛋白表达降低。[结论]花椒素WGX-50可通过调控OPG/RANK/RANKL通路增加骨质疏松小鼠骨密度、促进骨生成,减轻骨质疏松程度。
[Objective]To explore the effect of WGX-50 on osteoporosis in mice by regulating OPG/RANK/RANKL path⁃way.[Method]C57BL/6 mice were randomly divided into 5 groups:control group,osteoporosis group,low dose WGX-50 group,middle dose WGX-50 group,and high dose WGX-50 group.Osteoporosis model was established by gavage of retinoic acid(RA,90 mg/kg)once daily for 21 days.Mice in low dose,middle dose and high dose WGX-50 group were gavaged with WGX-50 at the dose of 0.5,1,and 2 mg/kg daily for 28 days,respectively.The mice in the control group and the model group were given normal saline by gavage.Bone mineral density(BMD)of mice in each group was detected by bone mineral density meter 24 hours after the last administration.The serum levels of bone metabolism markers(calcium and phosphorus)were ana⁃lyzed by colorimetry.The levels of serum bone formation markers(alkaline phosphatase and osteocalcin)were detected by en⁃zyme-linked immunosorbent assay.The pathological changes of femur tissue were analyzed by hematoxylin-eosin staining.Western blot was used to analyze the expression of OPG,RANK and RANKL proteins in mouse femoral tissue.[Result]Com⁃pared with the osteoporosis group,the femoral injury was alleviated,bone density increased(P<0.05),and the levels of bone formation markers(alkaline phosphatase and osteocalcin)were elevated(P<0.05)in the low-dose,medium-dose and high-dose WGX-50 group.Meanwhile,the levels of bone metabolism markers(calcium and phosphorus)were decreased(P<0.05),and the expression of OPG protein was increased while the expression of RANK and RANKL proteins was decreased.[Conclusion]Xanthoxylin WGX-50 can increase bone mineral density,promote bone formation and reduce the degree of oste⁃oporosis by regulating OPG/RANK/RANKL pathway in osteoporotic mice.
作者
涂艳
夏明
柳湘洁
TU Yan;XIA Ming;LIU Xiangjie(Department of Geriatrics,Liyuan Hospital,Tongji Medical College,Huazhong University of Science and Technology,Wuhan 430077,China)
出处
《生物技术》
2025年第6期787-791,760,共6页
Biotechnology
基金
湖北省中医药科研项目(ZY2025M008)。
