[Protective effect of ulinastatin on cerebral tissue in rats with lethal scald injury]

To explore the protective effects of ulinastatin on cerebral tissue in rats following lethal burn injury and its relationship with the expression of protective protein.

A total of 40 male Sprague-Dawley rats were randomly divided into scald and ulinastatin groups (n = 20 each). Both groups were subjected to 50% total body surface area third-degree burns. Immediately after scalding, 1 ml normal saline was injected intravenously in scald group while 1 ml saline containing ulinastatin (40 000 U/kg) in ulinastatin group. Then cerebral tissue was harvested for measuring the activities of neuron-specific enolase (NSE) by enzyme-linked immunosorbent assay (ELISA) at 6 h and 24 h post-injury. And the level of acetylated histone H3 was detected by Western blot and heat shock protein 70 (HSP70) by ELISA. The rates of tissue water content in heart were determined by dry/wet weight.

NSE and water content of cerebral tissue after 6 h injury in ulinastatin group were significantly lower than those in scald group ((146 ± 11) vs (156 ± 13) pg/ml, (77.3 ± 1.9)% vs (79.0 ± 2.2)%, both P < 0.05), the expressions of HSP70 and histone H3 after 6 h injury in ulinastatin group was significantly higher than those in scald group ((99 ± 19) vs (92 ± 13) pg/ml, (1.26 ± 0.37) vs (0.57 ± 0.23), both P < 0.05). The NSE content of cerebral tissue after 24 h injury in ulinastatin group was significantly lower than that in scald group ((141 ± 14) vs (159 ± 10) pg/ml, P < 0.05). And the water content of cerebral tissue, the expressions of HSP70 and histone H3 after 24 h injury had no significant inter-group differences ((75.9 ± 1.2)% vs (76.5 ± 1.4)%, (118 ± 17) vs (102 ± 16) pg/ml, (2.31 ± 0.27) vs (1.87 ± 0.31), both P > 0.05).

Ulinastatin significantly alleviates cerebral tissue injury in early stage of burn injury. And its protective effects may be due to the up-regulations of histone H3 and HSP70.