Objective: To investigate the effect of "Xuebijing injection" (Xuebijing in brief) on expression of hepatic high mobility group box-1 protein (HMGB1) and acute liver injury in rats with scald injury.
Methods: Seventy-eight rats were divided into sham scald group (n = 18), scald group (n = 30), and Xuebijing treatment group (n = 30). Rats in the latter 2 groups were subjected to 30% full-thickness scald injury followed with delayed resuscitation. These rats were sacrificed at 8th, 24th, and 72nd post-injury hour (PIH) to collect specimens. The hepatic pathological changes were observed. Serum levels of ALT and AST were detected. HMGB1 mRNA level in hepatic tissue was detected by the reverse transcription polymerase chain reaction. Protein relative expression quantity of HMGB1 in hepatic tissue was determined with Western blot and immunohistochemistry. Outcomes were denoted in integral absorbance ratio and absorbance value respectively.
Results: Massive infiltration of inflammatory cells in hepatic tissues was observed in scald group under light microscope, especially at 24th PIH, and it was decreased in quantity in Xuebijing treatment group. Compared with those of sham scald group, both mRNA and protein expressions of HMGB1 in hepatic tissue of scald group were significantly enhanced during 8-72 PIH (P < 0.05 or P < 0.01), along with markedly increased serum levels of ALT and AST (P < 0.05 or P < 0.01). Compared with those in scald group at 24h and 72nd PIH, hepatic HMGB1 mRNA expressions (0.75 +/- 0.12 vs. 0.60 +/- 0.15 and 0.78 +/- 0.11 vs. 0.55 +/- 0.07, respectively) and protein values (200 +/- 13 vs. 163 +/- 13 and 175 +/- 14 vs. 160 +/- 16, respectively) in Xuebijing treatment group were markedly down-regulated (P < 0.05 or P < 0.01), and serum levels of ALT and AST decreased in different degrees (P < 0.05 or P < 0.01).
Conclusions: HMGB1, the delay-appearing inflammatory mediator, is involved in the pathogenesis of inflammatory response in hepatic tissue in severely scalded rats. Treatment with Xuebijing can markedly down-regulate hepatic HMGB1 expression and protect liver against acute injury induced by delayed resuscitation.