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1.
Chinese Medical Journal ; (24): 3897-3903, 2013.
Article in English | WPRIM | ID: wpr-236142

ABSTRACT

<p><b>BACKGROUND</b>Hyperbaric oxygen (HBO) intervention is a main therapeutic method and the curative effect has been certified for spinal cord injury (SCI), but the mechanisms of the neuroprotective effect of HBO on SCI remain elusive. This study aimed to observe the change in expression of hypoxia-inducible factor-1α (HIF-1α) and vascular endothelial growth factor (VEGF) after SCI at different time points and to investigate the neuroprotective mechanism of HBO on SCI in rats.</p><p><b>METHODS</b>A total of 160 adult Sprague-Dawley rats, weighing between 250 and 300 g, were randomly assigned to four experimental groups (n = 40 per group). SCI group: SCI was created with a special NYU impactor of Allen's by a 25 gramcentimeter impacting energy on T10 of the spinal cord. SCI+HBO group: HBO therapy after SCI model was established. Sham operation (SH) group: only laminectomy of T10 and no impact on the spinal cord was done. SH+HBO group: HBO therapy after sham operation. The hindlimb functional recovery was evaluated using Basso, Beattie, and Bresnahan (BBB) score and the expressions of HIF-1α and VEGF were observed with fluorescent quantitation PCR and Western blotting method of six rats picked randomly from each group at different time points of 1, 3, 7, and 14 days after operation.</p><p><b>RESULTS</b>Rats in the SCI group and SCI+HBO group were paralyzed completely after operation with BBB 0-1 score. Rats in the SH group and SH+HBO group could walk after sham operation with BBB 20-21 score. The BBB score of rats in the SCI+HBO group (4.67±1.97 and 10.83±2.23) was higher than that in the SCI group (1.83±0.75 and 6.67±2.16) at 7 and 14 days time points obviously (P < 0.05). The expressions of HIF-1a and VEGF in the SCI group and SCI+HBO group were higher than in the SH group and SH+HBO group at any time point obviously (P < 0.05), while the SCI+HBO group presented the least expression of HIF-1α mRNA and protein (3.82±0.41 and 0.59±0.06; 2.26±0.41 and 0.37±0.05; 1.58±0.26 and 0.29±0.05) than that in the SCI group (6.36±0.58 and 0.76±0.07; 3.55±0.47 and 0.51±0.07; 2.27±0.39 and 0.40±0.06) respectively at 3, 7, and 14 days time points (P < 0.05) with significant difference and more expression of VEGF mRNA and protein (5.83±0.77 and 0.72±0.06; 4.59±0.51 and 0.63±0.06) than that in the SCI group (3.06±0.30 and 0.48±0.07; 2.25±0.24 and 0.39±0.09) respectively at 7 and 14 days time points (P < 0.05) with significant difference.</p><p><b>CONCLUSIONS</b>HBO could improve the hind limb functional recovery after SCI in rats. The elevation and duration of the expression of VEGF and the reduction of expression of HIF-1α by HBO intervention may be inversely related in the repair of damaged spinal cord and neuroprotective effect.</p>


Subject(s)
Animals , Rats , Hyperbaric Oxygenation , Methods , Hypoxia-Inducible Factor 1, alpha Subunit , Genetics , Metabolism , Rats, Sprague-Dawley , Spinal Cord Injuries , Genetics , Metabolism , Vascular Endothelial Growth Factor A , Genetics , Metabolism
2.
Chinese Medical Journal ; (24): 3904-3909, 2013.
Article in English | WPRIM | ID: wpr-236141

ABSTRACT

<p><b>BACKGROUND</b>Hyperbaric oxygen preconditioning (HBO) is a new method of ischemia preconditioning. In this study, we examined its effects on skin flap survival and the mechanisms involved.</p><p><b>METHODS</b>Thirty-six rats were divided into three groups: HBO preconditioning, control, and sham groups. An extended epigastric adipocutaneous flap based on the right superficial epigastric artery and vein was raised. A 3-hour period of flap ischemia was induced by clamping the pedicle vessels with a microvascular clamp. At the end of ischemia induction, the clamp was removed and the flap was resutured. Rats in the HBO preconditioning group were treated with HBO four times before surgery. Microcirculation in the skin flap was measured on postoperative days 1, 3 and 5. The size of the flap was measured on postoperative day 5, before the animals were sacrificed. Samples of the skin flap were prepared and stained with hematoxylin and eosin. The levels of tumor necrosis factor (TNF)-α, interleukin (IL)-1β, and IL-6 in the flap samples were measured.</p><p><b>RESULTS</b>Surviving flap size was significantly higher in the HBO preconditioning group compared with controls, with a reduced inflammatory response and increased perfusion. IL-1, TNF-α, and IL-6 levels in the HBO preconditioning group were lower than in controls.</p><p><b>CONCLUSIONS</b>HBO preconditioning improved flap survival in this ischemia-reperfusion rat model. The mechanisms responsible for this effect may relate to attenuation of the inflammatory response and increased flap perfusion following HBO preconditioning.</p>


Subject(s)
Animals , Male , Rats , Graft Survival , Hyperbaric Oxygenation , Methods , Ischemia , General Surgery , Microcirculation , Physiology , Rats, Sprague-Dawley , Skin , Surgical Flaps
3.
Chinese Journal of Industrial Hygiene and Occupational Diseases ; (12): 135-136, 2003.
Article in Chinese | WPRIM | ID: wpr-265035

ABSTRACT

<p><b>OBJECTIVE</b>To investigate the role of expression of platelet membrane glycoprotein CD31, CD61 and CD62p in the pathogenesis of decompression sickness.</p><p><b>METHODS</b>Mice were randomly divided into decompression sickness group and normal control group. The animals in decompression sickness group were exposed to 600 kPa compressed air for 60 minute, then they were rapidly decompressed to normal pressure in one minute. At 60th minute after reducing to normal pressure, the expression of CD31, CD61 and CD62p on platelet membrane in mice was measured by flow cytometry.</p><p><b>RESULTS</b>The mean fluorescence intensity of CD31, CD61 and positive percentage of CD62p on platelet membrane [(18.64 +/- 1.01), (271.06 +/- 24.25), (4.48% +/- 0.43%) respectively] in decompression sickness group were significantly increased compared with normal control group [(16.89 +/- 1.69), (234.09 +/- 15.96), (3.00% +/- 0.66%) respectively] (P < 0.05, P < 0.01).</p><p><b>CONCLUSION</b>Inadequately rapid decompression may induce up regulation of platelet membrane glycoprotein CD31, CD61 and CD62p expression in mice, which may lead to thrombosis.</p>


Subject(s)
Animals , Female , Mice , Blood Platelets , Chemistry , Decompression Sickness , Blood , Integrin beta3 , Blood , P-Selectin , Blood , Platelet Endothelial Cell Adhesion Molecule-1 , Blood
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