ABSTRACT
BACKGROUND:It has found that secretions of tumor necrosis factor α (TNF-α), interleukin 1β (IL-1β) and interleukin 6 (IL-6) are closely related to osteoporosis OBJECTIVE:To further investigate the levels of TNF-α, IL-1β and IL-6 of bone tissue in ovariectomized rats and their relationship with osteoporosis. METHODS: Sixty 3-month-old female Sprague-Dawley rats were randomly divided into control group and test group (n=30 per group). In the test group osteoporosis model was induced by ovariectomy folowed by intraperitoneal injection of aluminum nitride solution; while rats in the control group were given intraperitoneal injection of normal saline without ovariectomy. The experiment cycle was 12 weeks. One week after modeling, serum level of estradiol was tested, and the bone mineral density of rats measured with bone densitometry. In the meanwhile, the levels of TNF-α, IL-1β and IL-6 in bone tissue were detected to analyze the correlation between cytokines and bone mineral density. RESULTS AND CONCLUSION: The level of serum estradiol in the test group was significantly lower than that in the control group (P=0.007); the bone mineral density of the lumbar spine and femur in the test group was significantly lower than that in the control group (P=0.006, 0.004). Compared with the control group, the percentages of trabecular bone and osteoblast area within the visual field in the test group were significantly lower, while the osteoclast area within the visual field was significantly higher (P=0.037, 0.029, 0.044). Compared with the control group, the levels of TNF-α, IL-1β and IL-6 in the test group significantly increased (P=0.032, 0.031, 0.025). And the bone mineral density of the lumbar spine and femur was negatively correlated with the levels of TNF-α, IL-1β and IL-6 in the test group (P < 0.05). In conclusion, the osteoclast activity is enhanced by elevating the levels of TNF-α, IL-1β and IL-6 of bone tissue of ovariectomized rats, and increasing the percentage of osteoclast area within the visual field. Moreover, the percentages of trabecular bone and osteoblast area within the visual field have a decline, which accelerates the process of bone resorption and leads to the formation of osteoporosis. Subject headings:Ovary; Cytokines; Osteoporosis; Tissue Engineering
ABSTRACT
Objective To explore the effect of prevention and treatment on steroid-induced osteonecrosis of mice femoral head(ONFH) treated with metformin. Methods Thirty-six Kunming mice were randomly divided into three groups (n = 12):A (Control Group), B (Model Group)and C (Prevention Group). For producing ONFH mice models, did the intraperitoneal injection of horse serum (10 mL/kg) to B and C firstly. After two weeks, continuing the intraperitoneal injection of horse serum (5 mL/kg) again with the prednisolone intramuscularly [45 mL/(kg· day), totally for 5 days]. Meanwhile, feeding normal saline 10 mL/(kg·day) to B and feeding metformin hydrochloride [0.2 g/(kg·day)] to C. For A, mice were only given normal saline intramuscularly and intragastrically in equal quantity at the same time. The contents of serum cholesterol (TC), triglycerid (TG), plasma von willebrand factor (VWF) and plasminogen activator inhibitor 1 (PAI-1) were determined at the 2nd, 4th and 6th week after treatment. The micewere sacrificed at 2nd, 4th, and 6th weekafter treatment, and femoral heads were harvested to do histopathology analysis. Results The appearance and shape of the femoral head and the surface of cartilages were normal. The percentage of empty osteocyte lacunae in B was significantly higher than that in C (P 0.05). TC and TG contents in C were significantly lower than that in B in 2th、4th、6th weeek(P<0.05), and higher than that in A(P<0.05). VWF and PAI-1 level in C were significantly lower than that in B at 2nd and 4th week (P<0.05), but there were no statistical significance at 6th week. there were no statistical significance for the comparison between A and C. Conclusion Metformin can prevent steroid-induced ONFH by improving hyperlipemia, hypercoagulability and hypofibrinolysis, then effectively prevent osteonecrosis.