To discuss the influence of ulinastatin on cell apoptosis mediated by mitochondrial pathways in endotoxic myocardial injury rats.

A total of 24 male Wistar rats were randomly divided into three groups: the control group, the endotoxin group and the ulinastatin group, 8 rats in each group. Rats in the endotoxin group and ulinastatin group both received 10 mg/kg lipopolysaccharide by intraperitoneal injection, and rats in the ulinastatin group were given 20 000 U/kg ulinastatin 1 h after injection. Rats in the control group only injected equal dose saline at the same time. The pathological changes of myocardial tissues were observed. The serum troponin T (cTnT), and brain natriuretic peptide (BNP) levels were detected by enzyme-linked immunosorbent assay, and the myocardial cell apoptosis index was calculated. The expressions of Bcl-2, Bax, CytC, Caspases-3 proteins in myocardial cell were also determined by immunohistochemistry.

Rats in the endotoxin group had severe myocardial tissue damage, while rats in the ulinastatin group had a slightly myocardial tissue damage. The levels of cTnT, BNP all showed significantly differences among these three groups (F = 69.217, 18.250; all P < 0.05); the cTnT expressions [(20.3 ± 1.0), (18.7 ± 1.3), (12.2 ± 1.0) μg/L] and BNP expressions [(26.6 ± 1.4), (23.0 ± 2.4), (17.0 ± 1.6) μg/L] in the endotoxin and ulinastatin groups were much higher than those in the control group, and were highest in the endotoxin group (all P < 0.05). The myocardial cell apoptosis index in the ulinastatin group was much lower than that in the endotoxin group [(19.8 ± 1.7)% vs. (22.6 ± 1.2)%, t = 3.675, P = 0.020]. Meanwhile, the expression of Bcl-2 in the endotoxin and ulinastatin groups was much higher than that in the control group [(80.3 ± 3.8), (76.6 ± 2.90), (49.6 ± 3.9)], and was highest in the endotoxin group (all P < 0.05); the expressions of Bax [(70.8 ± 1.7), (80.0 ± 4.8), (99.7 ± 5.6)], CytC [(120 ± 5), (132 ± 3), (151 ± 7)] and Caspases-3 [(108.8 ± 4.0), (113.9 ± 5.2), (157.2 ± 2.5)] in the endotoxin and ulinastatin groups were lower than those in the control group, and were lowest in the endotoxin group (all P < 0.05).

Ulinastatin may reduce the occurrence of myocardial cell apoptosis by inhibiting the activation of mitochondrial pathways, and plays a certain protective role on endotoxic myocardial injury.