Thursday, September 27, 2018 2:05 PM–3:05 PM Section on Biologics and Basic Research Abstract Presentations: 129. Plastrum testudinis treating glucocorticoid-induce osteoporosis by down-regulating TNFR2

Abstract

BACKGROUND CONTEXT Glucocorticoid-induced osteoporosis (GIOP) is a systemic bone diseaseinduced by glucocorticoid (GC). The incidence of GIOP continues to rise with the widely use of GC, and GIOP has been identified as the most common type of secondary osteoporosis. Emerging evidence has demonstrated that bone fragility induced by GIOP is much more serious than that induced by postmenopausal osteoporosis, and GIOP has higher disability rate and mortality. Excessive or prolonged GC treatment has been considered to play a major role in inhibiting bone formation. However, the underlying mechanism of GIOP has not been confirmed. Thus, it is still an important and urgent project to find out how to research the mechanism and treat GIOP. PURPOSE To explore the effect of Plastrum Testudinis treating glucocorticoid-induce osteoporosis in Wnt/β-catenin pathway by down-regulating TNFR2.To explore the effect of Plastrum Testudinis treating glucocorticoid-induce osteoporosis in Wnt/β-catenin pathway by down-regulating TNFR2. STUDY DESIGN/SETTING Animal experiment:thirty 4-month-old SD rats were randomly divided into three groups: blank group, model group and Plastrum Testudinis group. The model group and the Plastrum Testudinis group were subcutaneously injected with dexamethasone, and were successfully gavaged with 0.9% sodium chloride solution and Plastrum Testudinis respectively. The lumbar spine (L1-6) were taken after 12 weeks. PATIENT SAMPLE No patients. Thirty 4-month-old SD rats were used in this study. OUTCOME MEASURES The mRNA expression of TNFR2, β-cantenin and GSK3β in the lumbar vertebra were detected by qPCR. The protein expressions of TNFR2, p-β-cantenin and p-GSK3β were detected by Western blot. Cell expeiment:CCK8 was used to detect the proliferation of BMSCs at different concentrations for 1,3,5,7 and 14 days. Osteogenesis was induced by selecting the best concentration. ALP and alizarin red staining were used to detect the effect of PTE on osteogenic differentiation of BMSCs. The expression of TNFR2, Β-cantenin, GSK3β mRNA expression, TNFR2, p-β-cantenin, p-GSK3β protein expression of turtle plate were detected by Werstern blot. METHODS Animal experiment: Thirty 4-month-old SD rats were randomly divided into three groups: blank group, model group and Plastrum Testudinis group. The model group and the Plastrum Testudinis group were subcutaneously injected with dexamethasone, and were successfully gavaged with 0.9% sodium chloride solution and Plastrum Testudinis respectively. The lumbar spine (L1-6) were taken after 12 weeks. The mRNA expression of TNFR2, β-cantenin and GSK3β in the lumbar vertebra were detected by qPCR. The protein expressions of TNFR2, p-β-cantenin and p-GSK3β were detected by Western blot. Cell expeiment:CCK8 was used to detect the proliferation of BMSCs at different concentrations for 1,3,5,7,14 days. Osteogenesis was induced by selecting the best concentration. ALP and alizarin red staining were used to detect the effect of PTE on osteogenic differentiation of BMSCs. The expression of TNFR2, Β-cantenin, GSK3β mRNA expression, TNFR2, p-β-cantenin, p-GSK3β protein expression of turtle plate were detected by Werstern blot. RESULTS Compared with the blank group, the level of β-catenin in the GIOP group was significantly decreased (P CONCLUSIONS Plastrum Testudinis can promote the proliferation, osteogenic differentiation and mineralization of BMSCs. It can effectively resist GIOP. The Plastrum Testudinis may resist the GIOP through down-regulating the Wnt /β-catenin pathway by inhibiting TNFR2. FDA DEVICE/DRUG STATUS This abstract does not discuss or include any applicable devices or drugs.