Abstract
Purpose: To investigate the protective effect of mollugin on glucocorticoid (GC)-induced osteoporosis in rats. Methods: A total of 30 female Sprague Dawley rats (weighing 180 to 200 g) were randomly assigned to five groups of six rats each: control, GC and mollugin groups (20, 40 and 80 mg/kg, respectively). Except for the control group, osteoporosis was induced in the rats by intramuscular administration of dexamethasone at a dose of 2.5 mg/kg twice weekly for nine weeks. Bone mineral density (BMD) and serum activities of tartrate-resistant acid phosphatase (TRAP) and specific alkaline phosphatase (ALP), and levels of collagen type I fragment (CTX) and osteocalcin were estimated. The effect of mollugin alone, and in the presence of PI3K/Akt inhibitor on the proliferation of bone marrow osteoblasts was investigated using 3-(4, 5-dimethylthiazol-2-yl)-2, 5-tetrazolium bromide (MTT) assay. Western blotting was used for determination of the expressions of p-Akt, Akt and cyclin D1 protein. Results: There were significant increases in body weights of rats in GC group, when compared with the control group. However, treatment with mollugin significantly reduced the body weights in a dosedependent manner (p < 0.05). The BMD was significantly reduced in GC group, relative to the control group (p < 0.05). Serum activities of TRAP and ALP were significantly higher in GC group than in control group, but were significantly reduced by mollugin treatment (p < 0.05). Serum level of CTX was significantly increased and osteocalcin reduced in the GC group, relative to control (p < 0.05). Osteoblast proliferation was significantly higher in the mollugin-treated groups. The expressions of p-Akt, Akt and cyclin D1 were significantly and dose-dependently higher in mollugin-treated groups (p < 0.05). There were more viable osteoblasts in the mollugin-treated groups than in the untreated group. However, treatment with mollugin in the presence of PI3K/Akt inhibitor significantly reduced their viability (p < 0.05). Conclusion: Mollugin has therapeutic potential for GC-induced osteoporosis via mechanism involving the PI3K/Akt pathway. Keywords: Mollugin, Osteoporosis, Bone, PI3K/Akt inhibitor, Osteoblast
Highlights
Osteoporosis is a metabolic disorder that results in decreases in the mass and quality of bone; and deterioration of bone architecture [1].Glucocorticoids (GCs) are used for the treatment of several chronic disorders such as cancer, gastrointestinal and autoimmune diseases [2]
A balance between functions of osteocytes and osteoblasts is responsible for bone remodeling
The body weights of rats increased significantly in GC group, relative to the control
Summary
Osteoporosis is a metabolic disorder that results in decreases in the mass and quality of bone; and deterioration of bone architecture [1]. A balance between functions of osteocytes and osteoblasts is responsible for bone remodeling These cells are the targets of glucocorticoids which induce apoptosis in them via a redox pathway [4]. The aim of this study was to investigate the protective effect of mollugin on glucocorticoid-induced osteoporosis in rats. A total of 30 female Sprague Dawley rats weighing between 180 and 200 g were procured from Shanghai Medical College, China. Sprague-Dawley rats of either sex aged 2 months or less were procured from Beijing Institute of Medical Sciences, China and used for primary osteoblast cell culture. Values of p < 0.05, were considered statistically significant
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