Objectives: To test whether myocardial apoptosis can be induced by traumatic fracture of lower limbs with hemorrhage, in order to lay a foundation of myocardial injury after traumatic fracture for the follow-up study.
Methods: Twenty SD rats were randomly divided into two groups, i. e. control group and trauma group(n=10). A rat model of traumatic hemorrhage was establish, and a traumatic model of the original generation of myocardial cell culture was constructed in vitro. The level of interleukin-2(IL-2),IL-6,IL-10 and tumor necrosis factor-α(TNF-α) in rat serum was detected by ELISA at 0, 1, 2, 4, 8, 12, 16, 24 and 48 hour to find the most significant point. The pathological cardiac injury in rats was observed by HE staining under a microscope, and the apoptosis of cultured cardiomyocyte in vitro was detected by TUNEL methods. The expressions of apoptosis gene,(Bcl-2) and Bax, in myocardium of rat and cultured cardiomyocyte in vitro were detected by Western blot and RT-PCR.
Results: At the 4th hour after trauma, IL-6 and IL-10 in the serum of rats reached its highest, IL-2 reached its lowest at the 8th hour after trauma, and TNF-αreached its highest at 1 hour after trauma, then all recovered to their normol level gradually. Myocardial HE staining indicated that cardiomyocyte was swelling, disordered derangement, inflammatory cell infiltrated; a large number of myocardial cell nuclei was dyedbrown in TUNEL test which proved that the apoptosis index increased (P<0.05). Western blot and RT-PCR results showed that the expression of pro-apoptotic gene Bax was up-regulated (P<0. 05), while expression of anti apoptosis gene Bcl-2 down-regulated (P<0.05).
Conclusions: The myocardial apoptosis can be induced by traumatic fracture of lower limbs with hemorrhage in rats, and then lead to myocardial injury.
Keywords: Bcl-2/Bax; myocardial apoptosis; traumatic hemorrhage.