ABSTRACT
BACKGROUND:Both osteopontin and leptin are closely linked to bone metabolism, therefore, which may be related to the attack of femoral head necrosis. OBJECTIVE:To study the correlation of serum osteopontin and leptin in the development of femoral head necrosis. METHODS:Thirty-one patients with femoral head necrosis (case group, including 11 cases of ARCO II, 10 of ARCO III, 10 of ARCO IV) and 10 healthy adults (control group) were selected as the research objects. Enzyme-linked immunosorbent assay was used to determine the levels of osteopontin and leptin in serum folowed by statistical analysis. RESULTS AND CONCLUSION:In the case group, the serum levels of osteopontin and leptin were significantly higher than those in the control group (P < 0.05). But the serum levels of osteopontin and leptin showed no correlation between the two groups. These findings indicate that the serum levels of osteopontin and leptin are both elevated in patients with femoral head necrosis, which maybe play a role in the pathogenesis of femoral head necrosis, but there is no obvious correlation.
ABSTRACT
Objective To observe the elimination of oxygen free radicals in rat myocardium mitochondria by diazoxide(DE) during different duration of hypothermic preservation.Methods The Langendorff model of isolated rat heart was used.After stored in 4℃ Celsior solution or Celsior solution containing 30 ?mol/L of DE for different duration(0,3,6,9 or 12h),the activity of the superoxide dismutase(SOD) and the content of maleic dialdehyde(MDA) in heart mitochondrial were measured.The myocardial mitochondria ultrastructure was also evaluated.Results(1) After hypothermic preservation,the activity of SOD was decreased,the content of MDA was increased.The ultrastructure of myocardium mitochondria was also destrored in preserved rat hearts in a time-dependent manner.(2) Compared with the corresponding Celsior solution hypothermic preservation groups,DE significantly improved the above indexes(SOD,MDA and myocardial mitochondria ultrastructure).Conclusion Diazoxide can protect rat myocardial mitochondria from long-term hypothermic preservation injury by direct elimination of oxygen free radials and enhancement of the activity of SOD.