[Expression and role of heat shock protein 70 and apoptosis related proteins in muscle tissue of pressure injury].

OBJECTIVE: To observe the phenomenon of apoptosis and expression of related proteins in injured muscle tissue during the formation of pressure injury, and to explore its mechanism of action on the pressure injury.

METHODS: Forty male Sprague-Dawley (SD) rats were divided into normal control group, 3, 5, 7 and 9 compression groups according to the random number table, with 8 rats in each group. The pressure injury models on the gracilis muscle of hind limbs were reproduced by using a way of cycle compression of ischemia/reperfusion (I/R) magnet. One cycle consisted of 12-hour compression, and followed by 12-hour release. The 5, 7, 9 compression groups were cut through after receiving 3 cycles. The normal control group did not receive any treatment. Muscle tissue specimens were harvested in the pressurized center at the end of the experiment (the same site for the normal control group), then the rats were sacrificed. The hematoxylin-eosin (HE) staining was used to examine the changes of muscle tissue morphology. The Hoechst 33258 staining was used to evaluate the apoptosis of muscle tissue. Western Blot was used to detect the expressions of heat shock protein 70 (HSP70), B-cell lymphoma-2 protein (Bcl-2) and Bcl-2 associated X protein (Bax).

RESULTS: (1) HE staining showed that the compressed tissues appeared different degrees of pathological degradation, and the change of tissue morphology was more serious with the increase of the compression cycle. (2) Hoechst 33258 staining showed that the nuclei of compressed tissue showed condensed, compact morphology and granular fluorescence, and the number of apoptotic cells increased with the increase of the compression cycle. (3) Western Blot showed that with the increase of the compression cycle the protein expressions of HSP70 and Bax were gradually increased, and the protein expression of Bcl-2 was gradually decreased. Compared with the normal control group, the protein expression of HSP70 in the 9 compression group was increased with statistically significant differences (HSP70/GAPDH: 1.78±0.21 vs. 0.55±0.17, P < 0.01). The protein expression of Bax in the 7 and 9 compression groups were increased with statistically significant differences (Bax/GAPDH: 0.96±0.09, 0.98±0.02 vs. 0.67±0.07, both P < 0.01). The protein expression of Bcl-2 in the 3, 5, 7 and 9 compression groups were significantly decreased (Bcl-2/GAPDH: 0.17±0.03, 0.13±0.03, 0.14±0.03, 0.10±0.02 vs. 0.36±0.04, all P < 0.05).

CONCLUSIONS: Apoptosis can be induced by I/R in pressure injury tissues. Apoptosis induced by HSP70 and apoptosis factors Bcl-2 and Bax may be involved in the formation of pressure injury.