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目的通过建立饮食诱导的高脂小鼠的模型,观察过氧化物酶体增生物激活受体γ(peroxisome proliferator-activated receptorγ,PPARγ)激动剂吡格列酮对肥胖小鼠的骨量变化的影响以及骨髓间充质干细胞(mesenchymal stem cell,MSCs)分化的情况,探讨PPARγ与MSCs分化之间的关系及可能的作用机制。方法建立饮食诱导的肥胖鼠模型,吡格列酮(10mg·kg-1.d-1)对肥胖小鼠进行灌胃,一个月后检测肥胖小鼠及灌胃组肥胖小鼠的葡萄糖耐量,骨密度及骨组织形态学,并取小鼠原代MSC进行培养,提取其RNA,利用实时定量PCR,检测在MSCs分化过程中成骨及成脂特异性基因的表达量。结果吡格列酮灌胃的肥胖小鼠胰岛素抵抗改善的同时,骨密度虽无明显改变,但骨组织形态学中成骨细胞周长百分率明显增加,原代MSCs的成骨分化基因的表达量明显增加而成脂基因明显下降。结论PPARγ改善胰岛素抵抗的同时,促使MSCs向成骨细胞分化的能力增强,向脂肪细胞分化的能力下降,PPARγ除直接参与调节MSCs的分化外,还可能通过间接作用在MSCs的分化过程中起重要作用。
OBJECTIVE: To establish a model of diet-induced hyperlipidemia in mice and observe the effects of peroxisome proliferator-activated receptorγ (PPARγ) agonist pioglitazone on bone mass in obese mice and the relationship between bone marrow To explore the relationship between the differentiation of mesenchymal stem cells (MSCs) and the differentiation of MSCs and its possible mechanism. Methods Fat-induced obese mice model was established. Pioglitazone (10 mg · kg-1.d-1) was orally administered to the obese mice. One month later, the obese and obese mice were inoculated with glucose, Bone histomorphology was taken and primary mouse MSCs were harvested for RNA extraction. Real-time quantitative PCR was used to detect the expression of osteogenic and adipogenesis-specific genes during MSCs differentiation. Results While insulin resistance was improved in pioglitazone-overexpressing mice, the BMD of osteoblasts significantly increased in bone histomorphology while the osteogenic differentiation gene expression of primary MSCs increased significantly Adipogenic genes decreased significantly. Conclusion PPARγ can improve the ability of osteoblasts to differentiate into osteoblasts and PPARγ to reduce the differentiation of adipocytes. PPARγ may play an important role in the differentiation of MSCs through indirect effects besides indirectly regulating the differentiation of MSCs effect.