Abstract
Postmenopausal diabetic women have a high risk of fractures. Salidroside has preventive effects on estrogen deficiency-induced osteoporosis and has hypoglycemic effects on diabetes in rats. However, whether salidroside inhibits bone loss in postmenopausal diabetic patients is still unknown. Here, we established a rat model of osteoporosis to investigate the protective effects of salidroside on bone loss induced by ovariectomy combined with diabetes, also investigating the underlying mechanisms. Two-month-old female Sprague-Dawley rats were divided into three equal groups (10 rats in each group): control group (with sham operation, treated with drug vehicle); OVX/T1DM group (ovariectomized diabetic rats); OVX/T1DM-SAL group, comprising ovariectomized diabetic rats treated with salidroside (20 mg/kg body weight) by gavage. The results showed that after 60 consecutive days of treatment, the bone mineral density (BMD) of OVX/T1DM-SAL increased significantly compared with the OVX/T1DM group (p < 0.01). The level of serum bone turnover markers, including alkaline phosphatase (ALP), cross linked c-telopeptide of type I collagen (CTX-1), osteocalcin, N-terminal propeptide of type I procollagen (PINP), and tartrate-resistant acid phosphatase 5b (TRACP 5b) were all increased in the OVX/T1DM group compared with the control (p < 0.01), and those were decreased by salidroside treatment. Meanwhile, the bone histopathological changes were also attenuated, and the bone marrow adipogenesis was inhibited in salidroside treated rats. Moreover, protein and mRNA ratio of bone osteoprotegerin (OPG)/receptor activator of nuclear factor-κB ligand (RANKL) was upregulated in ovariectomized diabetic rats by salidroside treatment. The results above indicated that the protective effect of salidroside on bone loss induced by ovariectomy and diabetes was mainly due to its ability to suppress bone turnover, inhibit bone marrow adipogenesis, and up-regulate the OPG/RANKL ratio.
Highlights
Postmenopausal osteoporosis is a metabolic bone disease characterized by loss of bone mass and deterioration of bone microarchitecture
OVX/Type 1 diabetes mellitus (T1DM)-SAL) suppressed the decrease in the body weight compared to that observed in vehicle-treated ovariectomized diabetic rats
We found that 60 days of salidroside treatment could effectively increase the bone mineral density (BMD), improve the bone tissue structure, and increase the bone volume, and trabecular thickness, and decrease the bone trabecular separation of ovariectomized diabetic rats, supporting our hypothesis that salidroside supplementation is beneficial in combined estrogen deficiency and T1DM induced bone loss
Summary
Postmenopausal osteoporosis is a metabolic bone disease characterized by loss of bone mass and deterioration of bone microarchitecture. It mainly affects older individuals, especially postmenopausal women, and results in hip and vertebral fractures. The main clinical symptoms of postmenopausal osteoporosis are reduced bone mineral density (BMD) and increased probability of Molecules 2018, 23, 2398; doi:10.3390/molecules23092398 www.mdpi.com/journal/molecules. Type 1 diabetes mellitus (T1DM) is a chronic disease characterized by the destruction of of fracture [4]. Type 1 diabetes mellitus (T1DM) is a chronic disease characterized by the destruction pancreatic beta cells, inadequate insulin production, and chronic hyperglycemia. T1DM is associated of pancreatic beta cells, inadequate insulin production, and chronic hyperglycemia. T1DM is with associated numerouswith complications, including disorders of bone metabolism [5], which have significant numerous complications, including disorders of bone metabolism [5], which have consequences for patients with
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