强骨抗萎膏通过调控MFN2及抑制内质网应激改善失重状态下大鼠骨丢失
Journal of Yunnan University of Chinese Medicine（2023）
北京中医药大学
Abstract
目的 观察强骨抗萎膏对尾吊大鼠骨细胞凋亡和内质网应激的影响,探讨强骨抗萎膏防治模拟失重状态下骨丢失的机制.方法 60 只SD大鼠分为对照组、模拟失重组、强骨抗萎膏组、阿仑膦酸钠组,骨疏康颗粒组,每组 12 只.采用尾部悬吊模拟失重状态,尾吊 28 d;对照组和模拟失重组给予每日等体积生理盐水灌胃,其它 3 组复制模型,分别每日给予中药强骨抗萎膏 2.4 g/kg,阿仑膦酸钠 0.007 g/kg,骨疏康颗粒 0.26 g/kg灌胃.持续给药 4 周后处死大鼠,TUNEL法检测骨细胞凋亡情况;Western blot法检测葡萄糖调节蛋白 78(GRP78)和线粒体融合蛋白 2(MFN2)表达,RT-PCR和Western blot检测骨组织中蛋白激酶R样内质网激酶(PERK),肌醇依赖性激酶 1α(IRE1α)、活化转录因子 6(ATF6)及C/EBP同源蛋白(CHOP)的基因和蛋白表达.结果 TUNEL结果显示模拟失重组骨细胞凋亡较对照组增加,强骨抗萎膏可抑制骨细胞凋亡.与对照组大鼠比较,模拟失重组PERK基因表达量明显增高(P＜0.05),强骨抗萎膏组较模拟失重组PERK基因表达量下降(P＜0.05);与对照组比较,模拟失重组的GRP78、PERK、CHOP和ATF6 蛋白含量明显增高(P＜0.05),MFN2 蛋白表达降低(P＜0.05),强骨抗萎膏组较模拟失重组GRP78、PERK、CHOP和ATF6 蛋白含量均明显降低(P＜0.05),MFN2 表达量升高.结论 强骨抗萎膏可以改善模拟失重大鼠骨细胞凋亡,通过抑制骨组织内质网应激相关因子GRP78、PERK、ATF6 和CHOP,上调MFN2 表达,从而改善失重条件下的骨丢失.
MoreKey words
weightlessness,bone loss,endoplasmic reticulum stress,MFN2,Qiang Gu Kang Wei Extraction
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