Abstract:

BACKGROUND: During hypoxia training, the body should bear the motor load and stay in the hypoxic environment outside.
OBJECTIVE: To observe the effect of hypoxia and hypoxia training on myocardial apoptosis and the expression of Bax and Bcl-2 in rats.
METHODS: Sixty Sprague-Dawley rats were randomly divided into six groups: normoxia group, 8 hours hypoxia group, 12 hours hypoxia group, normoxia training group, 8 hours hypoxia training group and 12 hours hypoxia training group, 10 rats in each group. The rats of normoxia training group, 8 hours hypoxia training group and 12 hours hypoxia training group were introduced to treadmill running on an incline of 0° at 25 m/min for 1 hour. After training, the rats of group 8 hours hypoxia group, 8 hours hypoxia training group, 12 hours hypoxia group and 12 hours hypoxia training group were exposed to hypoxic chamber with 12.5% volume fraction of oxygen (equal to altitude 4000 m) for 8 hours and 12 hours every day respectively. The course of the experiment was 4 weeks, 5 days every week. At 24 hours after the final experiment, the rats were treated with intraperitoneal anesthesia of sumianxin Ⅱ to obtain the samples, then hematoxylin-eosin staining, in situ terminal deoxyribonucleotide transferase-mediated dUTP nick end labeling method and protein immunohistochemistry methods were used to detect the myocardial apoptosis and the expression of Bax and Bcl-2 in rats.
RESULTS AND CONCLUSION: Compared with the normoxia group, the myocardial apoptosis index was significantly increased in the 24 hours hypoxia group, normoxia training group and hypoxia training group (P < 0.05); the myocardial apoptosis index in the 12 hours hypoxia training group was significantly higher than that in the normoxia training group and 8 hours hypoxia training group (P < 0.05). Compared with normoxia group, the expressions of Bcl-2, Bax and Bcl-2/Bax in the other five groups were significantly increased (P < 0.05); the expressions of Bcl-2, Bax and Bcl-2/Bax in normoxia training group were significantly higher than those in the 8 hours hypoxia group, and significantly lower than those in the 12 hours hypoxia group (P < 0.05); the expressions of Bcl-2, Bax and Bcl-2/Bax in the 12 hours hypoxia training group were significantly higher than those in the 12 hours hypoxia group and the 8 hours hypoxia training group (P < 0.05). Hypoxia and hypoxia training could induce the protein expressions of Bcl-2 and Bax in myocardial tissue. Hypoxia training was related with apoptosis rate and apoptotic index and pathological damage, especially the 12 hours hypoxia training. Bcl-2 and Bax participated in regulating the myocardial apoptosis.

Key words: tissue construction, tissue construction and bioactive factors, apoptosis, hypoxia, hypoxia training, hypoxia-inducible factor 1a, Bcl-2, Bax, myocardial cells, provincial grants-supported paper, tissue construction photographs-containing paper