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Abstract
BackgroundGlucocorticoid has been used extensively in clinical applications, because of its several pharmacologic actions, which include immunosuppression, anti-inflammation, anti-shock, and relief of asthma. However, the long-term or high-dose application of glucocorticoid can induce adverse effects such as osteoporosis, which is known in this case as glucocorticoid-induced osteoporosis (GIOP). It is a secondary osteoporosis that results in easy fracturing, and even disability. Therefore it became a thorny issue.MethodsThe rat model of glucocorticoid-induced osteoporosis (GIOP) was replicated to isolate BMSCs. Rats were assigned into four groups: normal, normal induction, GIOP, and GIOP induction. The growth cycle was monitored by using flow cytometry. Osteogenic differentiation was compared by using alkaline phosphatase (ALP) staining with a modified calcium cobalt method. The quantitative detection of osteoprotegerin and the receptor activator of nuclear factor kappa-B ligand (RANKL) was conducted by using enzyme-linked immunoassay. Finally, renal Klotho mRNA expression was assessed by using RT-PCR.ResultsBMSC proliferation was reduced in GIOP rats. The ALP-positive expression of normal BMSCs to the osteogenic induction solution was stronger than that of BMSCs from GIOP rats (P < 0.01). Osteoprotegerin expression was significantly higher in the normal induction group than in the normal, GIOP (P < 0.01), and GIOP induction groups (P < 0.05). RANKL expression was significantly higher in the normal induction group than in the other groups (P < 0.01) and significantly higher in the normal group than in the GIOP and GIOP induction groups (P < 0.01). RT-PCR analysis showed that renal Klotho mRNA expression was significantly reduced in the GIOP group compared with the normal group (P < 0.01).ConclusionBMSC proliferation, osteogenic differentiation, and reactive activity to an osteogenic inductor were reduced in GIOP rats. Klotho mRNA expression decreased during GIOP induction.
Highlights
Glucocorticoid has been used extensively in clinical applications, because of its several pharmacologic actions, which include immunosuppression, anti-inflammation, anti-shock, and relief of asthma
The present study aims to investigate the influence of GC on the osteogenic differentiation of rat bone marrow-derived mesenchymal stem cells (BMSCs) and determine the pathological mechanism of GCs to establish a foundation for the prevention of glucocorticoid-induced osteoporosis (GIOP) by Chinese medicine
Comparison between the BMSC growth cycles for normal and GIOP rats Approximately 10.10% and 5.82% of BMSCs in normal and GIOP rats were arrested at S + G2 + M, respectively (Figure 1A and B)
Summary
Glucocorticoid has been used extensively in clinical applications, because of its several pharmacologic actions, which include immunosuppression, anti-inflammation, anti-shock, and relief of asthma. It is a secondary osteoporosis that results in easy fracturing, and even disability. OP can increase the incidence of fractures and is one of the Osteoblast (OBs) and fat cells originate from bone marrow-derived mesenchymal stem cells (BMSCs) and have the same cell phenotype. GCs promote and inhibit the differentiation of BMCSs into lipocytes and OBs, respectively, leading to coupling imbalance between OBs and osteoclasts. This phenomenon causes bone loss and OP [4]. The present study aims to investigate the influence of GC on the osteogenic differentiation of rat BMSCs and determine the pathological mechanism of GCs to establish a foundation for the prevention of glucocorticoid-induced osteoporosis (GIOP) by Chinese medicine
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