Effects of pioglitazone on BMSCs differentiation into osteoblastic lineages
Haining Fang
Abstract
Haining Fang
Abstract
Objective To observe the effects of glucose and pioglitazone on rat bone-marrow stromal cells (BMSCs) differentiation into osteoblastic lineages in vitro and to investigate the mechanism of them. Methods Obtain bone-marrow stromal cells from long bone marrow of rat,and interfere them into osteoblasts with different doses of glucose concentration (5.6, 25, and 50 mmol·L-1),alone, with pioglitazone (0.1 μg·mL-1) in the presence of an osteogenic medium. The rate of mineralization would be examined by staining of mineralized nodules with Alizarin red S, and the difference of alkaline phosphatase(ALP), bone gla protein and Runx2 between interblocks was examined by real time PCR. After 21 d of culture. Results The rate of mineralization cut down significantly in higher concentration glucose. Compared with the control group(5.6 mmol·L-1).The rate of mineralization decreased 21% in 25 mmol·L-1 glucose group,and it deceased 55% in 50 mmol·L-1 glucose group(P0.01). The mRNA expression of ALP, BGP and Runx2 also cut down significantly in higher concentration glucose. Compared with the control group(5.6 mmol·L-1),them decreased 21%, 12% and 15% in 25 mmol·L-1 glucose group(P0.05);and them also cut down significantly in 50 mmol·L-1 glucose group(P0.05). In triconcentration of glucose, compared with the corresponding control group,the rate of mineralization decreased 20%, 25%, 25% with pioglitazone(P0.05),and the mRNA expression of ALP,BGP and Runx2 also cut down significantly with pioglitazone(P0.01).Conclusion High concentration glucose inhibited the differentiation of BMSCs into osteoblastics, this observation provide a potential mechanisms of diabetes-induced osteoporosis. Pioglitazone also inhibited osteoblastic of BMSCs, it causes decrease of bone mass by inhibiting osteoblastic and promoting adipogenesis diffenrentiation and it may be the important potential pathogenisis of pioglitazone caused by osteoporosis.
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Objective To observe the effects of glucose and pioglitazone on rat bone-marrow stromal cells (BMSCs) differentiation into osteoblastic lineages in vitro and to investigate the mechanism of them. Methods Obtain bone-marrow stromal cells from long bone marrow of rat,and interfere them into osteoblasts with different doses of glucose concentration (5.6, 25, and 50 mmol·L-1),alone, with pioglitazone (0.1 μg·mL-1) in the presence of an osteogenic medium. The rate of mineralization would be examined by staining of mineralized nodules with Alizarin red S, and the difference of alkaline phosphatase(ALP), bone gla protein and Runx2 between interblocks was examined by real time PCR. After 21 d of culture. Results The rate of mineralization cut down significantly in higher concentration glucose. Compared with the control group(5.6 mmol·L-1).The rate of mineralization decreased 21% in 25 mmol·L-1 glucose group,and it deceased 55% in 50 mmol·L-1 glucose group(P0.01). The mRNA expression of ALP, BGP and Runx2 also cut down significantly in higher concentration glucose. Compared with the control group(5.6 mmol·L-1),them decreased 21%, 12% and 15% in 25 mmol·L-1 glucose group(P0.05);and them also cut down significantly in 50 mmol·L-1 glucose group(P0.05). In triconcentration of glucose, compared with the corresponding control group,the rate of mineralization decreased 20%, 25%, 25% with pioglitazone(P0.05),and the mRNA expression of ALP,BGP and Runx2 also cut down significantly with pioglitazone(P0.01).Conclusion High concentration glucose inhibited the differentiation of BMSCs into osteoblastics, this observation provide a potential mechanisms of diabetes-induced osteoporosis. Pioglitazone also inhibited osteoblastic of BMSCs, it causes decrease of bone mass by inhibiting osteoblastic and promoting adipogenesis diffenrentiation and it may be the important potential pathogenisis of pioglitazone caused by osteoporosis.
Key concepts: Pioglitazone, RUNX2, Alkaline phosphatase, Mineralization (soil science), Stromal cell, Internal medicine, Endocrinology, Chemistry