| Objective: Osteoporosis is a kind of systemic metabolic osteopathy characterized by low bone mass,damage of bone microstructure,increase of bone fragility and easy occurrence of brittle fracture,which will seriously affect the quality of life of patients.One of the reasons for osteoporosis is the long-term use of glucocorticoids.Glucocorticoids are widely used in medicine.At present,studies have shown that the abuse of glucocorticoids is widespread in the country.Therefore,the incidence rate of glucocorticoid induced osteoporosis is only third,which is next to menopausal osteoporosis and senile osteoporosis.Autophagy is a common and important life phenomenon in eukaryotic cells.It is widely involved in a variety of physiological and pathological processes,and has become a research hotspot of programmed cell death in recent years.It is of great significance to study the mechanism and effect of autophagy in glucocorticoid induced osteoporosis.Therefore,this study compared the expression of beclin-1,p62,lc3 b in bone tissue of rats with glucocorticoid osteoporosis and normal rats,to explore the role and significance of autophagy in glucocorticoid osteoporosis.Methods: 1.Twenty four 8-week-old female SD rats were reared in SPF animal feeding room of Benxi experimental center,Shengjing Hospital Affiliated to China Medical University.After one week of adaptive feeding,the rats were randomly divided into two groups,12 rats in each group,the osteoporosis model group and the control group.The rats in osteoporosis group were injected with dexamethasone 5mg / kg every two weeks,and the rats in the control group were injected with the same dose of normal saline,and the lower limbs were injected alternately.After 6 months of intervention,the rats in the two groups were killed after weighing,and the bone tissues of the distal femur and the proximal tibia were selected.After removing the redundant soft tissues,they were fixed,decalcified and pathological sections were made.2.HE staining was used to detect the gross structure of bone trabeculae in metaphysis of distal femur and proximal tibia,and immunohistochemical staining was used.The expression of beclin-1,p62 and lc3 b in bone cells of the two groups were detected and compared.Results: 1.HE staining results showed that compared with the control group,the trabeculae of tibial metaphysis in osteoporosis group became thinner,the number of trabeculae decreased significantly,and the arrangement was disordered.The number of vacuole fat cells increased significantly.2.The results of immunohistochemistry showed that the expression of beclin-1 and lc3 b in the epiphysis of tibia in the experimental group was divided into: beclin-1 protein(116.54 ± 5.34),lc3 b protein(87.65 ± 3.87),becline-1 protein(56.97 ± 3.97)and lc3 b protein(48.14 ± 3.24)were significantly higher than that in the control group;p62 protein(78.53 ± 2.36)in the experimental group was significantly lower than that in the control group(146.53 ± 3.59)(P<0.05)。Conclusion: 1.The rat model of glucocorticoid osteoporosis was established successfully.Compared with the control group,the weight of the rats in the osteoporosis group was generally increased,indicating that the rats were generally obese after dexamethasone intervention and had obvious osteoporosis.2.There was an increase of autophagy level in the bone cells of the rats with glucocorticoid osteoporosis,and the level of autophagy might be sugar The incidence and development of corticosteroid osteoporosis. |
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