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Effects of hyperbaric oxygen on TF、TNF-α in the rabbit model of steroid-induced avascular osteonecrosis of femoral head

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Author:
No author available
Journal Title:
CHINESE JOURNAL OF NAUTICAL MEDICINE AND HYPERBARIC MEDICINE
Issue:
2
DOI:
10.3760/cma.j.issn.1009-6906.2011.02.007
Key Word:
股骨头缺血坏死;激素;组织因子;肿瘤坏死因子;高压氧;Avascular necrosis of the femoral head;Hormone;Tissue factor;Tumor necrosis factor;Hyperbaric oxygen

Abstract: Objective To investigate dynamic changes in serum TF and TNF-α in the rabbit model of steroid-induced avascular osteonecrosis of femoral head ( SANFH) and also to explore the mechanism of SANFH, as well as effects of hyperbaric oxygen ( HBO) on SANFH. Methods Seventy-eight New Zealand male rabbits were randomly divided into 3 groups:the normal control (group N) (7 animals), the model group (group M) (41 animals) and the HBO group (group H) (30 animals). The model group was subdivided into the immediate model group (the M0 group) (10 animals), the two-week model group (the M2 group) (10 animals), the four-week model group (the M4 group) (10 animals) and the six-week model group (the M6 group) (11 animals). The HBO group was further divided into the 2-week HBO therapy group (HBO2) (7 animals), the 4-week HBO therapy group (HBO4) (11 animals) and the 6-week HBO therapy group (HBO6) (12 animals). Through injection of endotoxin and methyl-prednisolone, rabbits in the group HBO2, HBO4 and HBO6 received HBO therapy 1 hour daily from the second day of the experiment. The durations of HBO therapy were 2 weeks ( HBO2), and 4 weeks respectively. The animals were sacrificed after blood samples were taken at respective blood collection time. Then, levels of TF, TNF-α in the serum were measured and the histological changes in the femoral heads were observed. Results Levels of TF and TNF-α in group M0 increased significantly, when compared with those of group N (P <0. 05 or P <0.01), while for the HBO subgroups the expression of TF and TNF-α measured at the same time points all decreased, when compared with that of the model subgroups (P<0. 05 or P <0.01). To elaborate, TF levels in group M2 and M4 were much higher than those in group HBO2 and HBO4 ( P<0. 01 ). TF level in group M6 was higher than that in group HB06 ( P < 0.05). TNF-α in group M0 also increased significantly, when compared with that in group N( P <0.01). TNF-α levels in group M2 and M6 were also much higher than those in group HBO2 and HBO6 ( both P <0. 01 ). TNF-α in group M4 was higher than that in group HBO4 (P<0.01). Histological examination revealed that tissues of the femoral heads in group N were normal, osteonecrosis and thrombus could be noted in group M2 and M4, hyperplasia fibrosis could be found in group M6, and osteonecrosis in HBO2 and HB04 groups seemed less severer than that in M2 and M4 groups, no thrombi in HBO2, HBO4 groups were noted, and growth of new bones were detected in HBO4 and HBO6. Conclusions The levels of TF and TNF-α levels increased in the rabbit model of SANFH, inducing blood coagulation. Thrombosis at the femoral heads was one of the causes of SANFH. HBO therapy could inhibit the release of TF and TNF-α, thus improving the abnormality of blood coagulation and enhancing treatment of osteonecrosis.

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