Expression and significance of bcl-2 and bax genes during the development of traumatic avascular necrosis of the femoral head
- VernacularTitle:创伤性股骨头缺血坏死过程中凋亡调控基因bcl-2、bax的表达及意义
- Author:
Xinwen QI
;
Rongze AN
- Publication Type:Journal Article
- From:
Chinese Journal of Tissue Engineering Research
2007;0(37):-
- CountryChina
- Language:Chinese
-
Abstract:
BACKGROUND: Osteocytes are the main function cells in the femoral head. Therefore, the study of the apoptosis of osteocytes and the correlative stress genes has become the research focus for exploring the pathomechanism underlying avascular necrosis of femoral head. OBJECTIVE: To observe the expression changes of bcl-2 and bax genes during the development of traumatic avascular necrosis of femoral head in rabbits, and explore the pathomechanism underlying this disease. DESIGN, TIME AND SETTING: An animal observational experiment was performed at the Central Laboratory of Zhuhai Campus of Zunyi Medical College between December 2007 and September 2008. MATERIALS: A total of 35 New Zealand rabbits were randomly divided into 7 groups, namely, the control group and the experiment group which are subdivided into six ones at the time points of 3, 6, 12, 24, 48 and 96 hours postischemia respectively , with 5 animals in each group. METHODS: Rabbits in the experiment group were given an open surgery of interrupting the blood supply of their femoral heads to lead to avascular necrosis; rabbits in the control group only received skin incision and muscle-sparing ended in their joint capsules. Osteocytes, Bcl-2 and Bax proteins in femoral heads were determined and compared at different time points postischemia. MAIN OUTCOME MEASURES: Lacunae changes of osteocytes in femoral heads were detected with hematoxylin-eosin (HE) staining method, and the expression of Bcl-2 and Bax proteins with immunohistochemistry staining methods (ABC methods), after 3, 6, 12, 24, 48 and 96 hours of ischemia respectively. RESULTS: According to HE staining, ischemia of 12 hours or less resulted in no osteocyte lacunae change; after 48 hours of ischemia, parts of osteocytes and osteoblasts disappeared; at hour 96 postischemia, the percentage of empty osteocyte lacunae was higher obviously than that at hour 48 or that in the control group (P
