Ferrostatin-1抑制高糖诱导的小鼠BMSC铁死亡并防治糖尿病骨质疏松
Ferrostatin-1 inhibits iron death of BMSC induced by high glucose in mice and treats diabetic osteoporosis
  
DOI:10.3969/j.issn.1006-7108.2023.10.005
中文关键词:  Ferrostatin-1  BMSC  铁死亡  糖尿病性骨质疏松
英文关键词:ferrostatin-1  BMSC  iron death  diabetic osteoporosis
基金项目:自治区卫生健康青年医学科技人才专项(WJWY-202135);自治区创新环境(人才、基地)建设专项联合基金(2021D01C213)
作者单位
涂来勇1,3 夏力4 田峰1,3 胡铜1,2,3 吴昊天1,2,3 祖力卡尔·阿地力1,2,3 赵疆1,3 * 1.新疆维吾尔自治区中医医院新疆 乌鲁木齐 830099 2.新疆医科大学新疆 乌鲁木齐 830000 3.新疆维吾尔自治区中医药研究院新疆 乌鲁木齐 830000 4.武警新疆总队医院外二科新疆 乌鲁木齐 830000 
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中文摘要:
      目的 探讨铁死亡抑制剂对糖尿病骨质疏松模型小鼠的治疗作用。方法 体外研究采用Ferrostatin-1干预小鼠骨髓间充质干细胞(BMSC)成骨分化,并检测成骨分化及铁死亡标志基因的表达;体内研究采用Ferrostatin-1干预糖尿病骨质疏松模型小鼠,并检测小鼠空腹血糖、体重、松质骨相关参数。结果 体外研究显示,与对照组相比,高糖环境下,BMSC的成骨分化能力被抑制,Ferrostatin-1(10 μmol/L)能够挽救高糖抑制的成骨分化,差异存在统计学意义。体内研究显示,与对照组相比, Ferrostatin-1可以有效降低糖尿病模型小鼠的空腹血糖,并增加体重,且差异均有统计学意义。与对照组相比,糖尿病模型鼠骨小梁面积百分数、骨小梁宽度、骨小梁数量下降,且差异有统计学意义;与模型组相比,Ferrostatin-1治疗组骨小梁面积百分数、骨小梁宽度、骨小梁数量增加,且差异有统计学意义。结论 Ferrostatin-1抑制高糖高脂环境下的BMSC铁死亡,防治糖尿病性骨质疏松。
英文摘要:
      Objective To investigate the therapeutic effect of iron death inhibitor on diabetic osteoporosis model mice. Methods Ferrostatin-1 was used to intervene the osteoblast differentiation of bone marrow mesenchymal stem cells (BMSC) in vitro, and the expression of osteogenic differentiation and iron death marker genes was detected. Ferrostatin-1 was used to intervene diabetic osteoporosis model mice, and fasting blood glucose, body weight and cancellous bone related parameters were detected. Results In vitro study, compared with the control group, the osteogenic differentiation ability of BMSC was inhibited under high glucose, and ferrostatin-1 (10 μm) could rescue the osteogenic differentiation inhibited by high glucose, and the difference was statistically significant. In vivo studies showed that ferrostatin-1 could effectively reduce fasting blood glucose and increase body weight in diabetic mice compared with the control group, and the differences were statistically significant. Compared with the control group, the percentage of trabecular bone area, the width of trabecular bone and the number of trabecular bone in the diabetic model mice decreased, and the differences were statistically significant. Compared with the model group, the percentage of trabecular area, the width of trabecular bone and the number of trabecular bone in the ferrostatin-1 treatment group were increased, and the differences were statistically significant. Conclusion Ferrostatin-1 inhibits iron death in BMSC under high glucose and fat environment and prevents diabetic osteoporosis.
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