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| 二甲双胍抑制破骨分化改善糖尿病模型鼠骨量的研究 |
| Effect of metformin on bone mass in diabetic mice by inhibiting osteoclast differentiation |
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| DOI：10.3969/j.issn.1006-7108.2022.08.017 |
| 中文关键词: 二甲双胍 破骨分化 糖尿病 骨量 |
| 英文关键词:metformin osteoclast differentiation diabetes mellitus bone mass |
| 基金项目:基金项目：省部共建中亚高发病成因与防治国家重点实验室开放课题项目（SKL-HIDCA-2020-ZY19） |
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| 中文摘要: |
| 摘要：目的 探讨二甲双胍对骨髓源性巨噬细胞（BMDM）破骨分化的影响，并观察二甲双胍对糖尿病模型鼠骨量的改善作用。方法 在体外实验中，通过梯度浓度的二甲双胍干预RANKL诱导的大鼠BMDM破骨分化，并检测破骨分化标志基因Nfatc1、Ctsk、C-fos、Traf6及相应标志蛋白的表达；在体内实验中，将24只8周龄大鼠随机分为对照组、糖尿病模型组（模型组）、糖尿病模型组+二甲双胍干预组（治疗组），每组各8只，其中对照组与模型组行生理盐水灌胃，治疗组使用二甲双胍灌胃，治疗时间为3个月，检测大鼠体重、空腹血糖，并检测各组大鼠骨量的变化。结果 在体外实验中，二甲双胍显著抑制大鼠BMDM破骨分化，并呈浓度依赖性，显著下调破骨分化标志基因Nfatc1、Ctsk、C-fos、Traf6的表达（P＜0.05），显著下调破骨分化标志蛋白C-FOS、NFATC1、TRAF6、CTSK的表达；在体内实验中，模型组相比较于对照组，体重减轻、空腹血糖上升、骨量降低；治疗组相比较于模型组，体重增加、空腹血糖降低、骨量增加。结论 二甲双胍能够抑制破骨分化，在增加体重、降低空腹血糖的同时，可以减少骨表面的破骨细胞数量和面积，改善骨量。 |
| 英文摘要: |
| Abstract: Objective To investigate the effect of metformin on osteoclast differentiation of bone marrow derived macrophages (BMDM), and to observe the effect of metformin on improving bone mass in diabetic mice. Methods In vitro experiments, metformin at gradient concentration interfered with osteoclast differentiation of RANKL-induced rat BMDM, and the expression of osteoclast differentiation marker genes Nfatc1, Ctsk, C-FOS, Traf6 and corresponding marker proteins were detected. In vivo experiment, only 8 weeks 24 rats were randomly divided into control group, diabetic model group (model group), the diabetic model group + metformin intervention group (treatment group), each group of eight, saline lavage with control group and model group, treatment group using metformin to fill the stomach, treatment time for 3 months, detection of rat body weight, fasting blood glucose. The changes of bone mass in each group were detected. Results Metformin significantly inhibited osteoclast differentiation of rat BMDM in a concentration-dependent manner, and significantly down-regulated the expression of marker genes Nfatc1, Ctsk, C-FOS and Traf6 (P<0.05). The expression of osteoclast differentiation marker proteins C-FOS, NFATC1, TRAF6 and CTSK were significantly down-regulated. In vivo experiment, compared with the control group, the model group lost weight, fasting blood glucose increased, and bone mass decreased, while the treatment group gained weight, fasting blood glucose decreased, and bone mass ameliorated. Conclusion Metformin can inhibit osteoclast differentiation, increase body weight, decrease fasting blood glucose, and reduce the number and area of osteoclasts on the bone surface, and improve bone mass. |
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