摘要
目的探讨恒古骨伤愈合剂(OK)通过磷脂酰肌醇-3激酶(PI3K)/蛋白激酶B(AKT)/糖原合成酶(GSK)-3β信号通路治疗绝经后骨质疏松(PMOP)的作用。方法 12月龄雌性实验树鼩60只,随机分成正常组、PMOP模型组、PMOP模型加低剂量OK组、PMOP模型加中剂量OK组、PMOP模型加高剂量OK组及PMOP模型加阳性药对照组,每组10只。通过摘除两侧卵巢制备PMOP树鼩模型,检测各组树鼩骨密度(BMD),收集血清和骨骼,检测血清雌二醇(E2)、骨碱性磷酸酶(BALP)、骨钙素(OC)和Ⅰ型原胶原N-端前肽(PINP)浓度;分别采用RT-qPCR和Western印迹法检测PI3K、AKT和GSK-3β的表达水平。结果 OK能提高模型组的BMD及其血清中E2、BALP、OC和PINP浓度,并且OK还能上调PI3K的表达水平和AKT的磷酸化水平,下调GSK-3β的表达水平,疗效均具有剂量依赖性。结论 OK可以通过促进骨细胞增殖的作用缓解PMOP,这种治疗作用可能是通过调控PI3K/AKT/GSK-3β信号通路实现的。
Objective To investigate the effects of osteoking (OK) on the postmenopausal osteoporosis via the PI3K/AKT/GSK-3β signal pathway.Methods 60 female experimental tree shrews were randomly divided into 6 groups.The BMD of all the shrewswere determined,the concentrations of E2,BALP,OC and PINP were detected. The expression levels of PI3K,AKT and GSK-3β weredetermined by RT-qPCR and Western blot respectively. Results OK enhanced the BMD,and increased the concentrations of serum E2,BALP,OC and PINP,moreover OK upregulated the expression level of PI3K and the phosphorylation level of AKT,downregulat-ed the expression level of GSK-3β,and all the therapeutic effects had a dose-dependent manner. Conclusions OK could alleviatePMOP by promoting the role of bone cell proliferation,which might be implicated in regulating PI3K/AKT/GSK-3β signaling pathway.
作者
郑红
赵宏斌
袁鑫
吴超
角建林
唐薇
ZHENG Hong;ZHAO Hong-Bin;YUAN Xin(Department of Laboratory Animal Science,Kunming Medical University,Kunming 650500,Yunnan,China)
出处
《中国老年学杂志》
CAS
北大核心
2019年第3期626-630,共5页
Chinese Journal of Gerontology
基金
国家自然科学基金资助项目(81460647)
云南省应用基础研究计划项目(2012FB022
2014FB033)
