| OBJECTIVE To find out the change of plasma adiponectin level after modeling ,confirm that the application of large doses of glucocorticoids can cause avascular necrosis of femoral head , and evaluate the effect of direct injection of recombinant rat adiponectin into the hip joint on steroid-induced avascular necrosis of femoral head in rats, and further understand the relationship between adiponectin and bone metabolism,provide some ideas for clinical prevention and treatment of bone metabolic diseases .METHODS Forty Sprague Dawley female rats with body weight of (250±30) grams were randomly divided into control group (A group=8) and model group. The rats in the model group were injected prednisolone acetate 24.5 mg/kg twice a week for 6 weeks to establish the early steroid-induced avascular necrosis models. Rats in the control group were received isodose physiological saline. 2ml blood were collected from each rat for the adiponectin ELISA testing before and after modeling .Then all the rats in the model group were randomly divided into B, C, D groups with 8 rats in each group . C, D groups were injected with 1μg, 10μg of recombinant adiponectin into the right hip respectively, B group were injected with isodose physiological saline. The right femoral head of 4 groups were examinated by X ray 4 weeks after the injection .The extent of necrosis and repair were observed under a light microscope. Trabecular bone area, empty bone lacuna rate, vascular number were analyzed and the expression of TNF-αof the femoral head was detected by immunohistochemical method. RESULTS1. Plasma adiponectin levels of control group did not change significantly before and after modeling (P>0.05), while plasma adiponectin levels of model group drop to (5.088±0.463) ng / ml after modeling, significantly lower than the level before modeling (8.84±0.662) ng / ml (P<0.01).2. The results of X-ray examination showed that control group was normal. B, C groups showed density of femoral head was uneven and trabecular bone was fuzzy; Bone density of D group was normal .3. Bones of A group were hard, bones of B group were significantly osteoporosis, bone hardness of C,D groups were between A,B groups.4. Light microscopy showed that trabecular bone, bone lacunae, vascular number of A group are normal. Empty lacunae rate :(30.600±6.060)%, percentage of trabecular bone area:(0.219±0.019), average number of subchondral vessels :(1.75±0.71) of B group compared with control group were significantly different (P>0.01). Empty lacunae rate :(12.900±3.214)%, percentage of trabecular bone area :(0.351±0.048), percentage of subchondral vessels: (3.75±1.17) of D group were significantly superior to the results of B group (P<0.01), the differences between C group and B group were not significant (P>0.05 ).5. The expression of TNF-αin B group was higher than A, C, D three groups (P<0.01). OPG expression in group B was lower than A, D group (P <0.01), there was no significant difference between B and C group (P>0.05).CONCLUSION1. Long-term use of high-dose glucocorticoids can lead to plasma adiponectin level decrease in rats.2. Direct injection of recombinant rat adiponectin into hip joint can promote the repair of steroid-induced avascular necrosis of femoral head and affect the local expression of TNF-αand OPG in rats in a dose-dependent.
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