Enhancing Mechanisms of p38MAPK/NF-κB in Regulating Post-Debridement Inflammatory Response during the Shock Period in Burned Rats.

Abstract

This study aimed to observe the temporal changes in inflammatory factors and explore the mechanisms regulating inflammation during the shock period following debridement in rats. A burn model was established in SD rats using a 30% total body surface area III-degree scald. Rats were divided into three groups: control group, debridement group (12 hours post-burn debridement with heterograft skin coverage), and sham surgery group (simulated debridement with autograft skin coverage). Serum samples were collected at 12, 24, 48, 72, and 96 hours post-injury to assess levels of inflammatory factors and proteins related to the p38 MAPK/NF-κB pathway. The levels of lipopolysaccharide-binding protein (LBP), high-mobility group box 1 (HMGB1), interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α), and IL-10 in the control group peaked between 12 and 48 hours post-injury, while HMGB1 increased gradually, peaking at 96 hours. Compared to the control group, both the debridement and sham surgery groups showed significant reductions in these inflammatory factors (P<0.01 or P<0.05), except for LBP. Liver p38MAPK levels showed no significant difference between groups, but phosphorylated p38MAPK and NF-κB levels significantly decreased (P<0.05 or P<0.01). In the debridement group, intra-group comparisons revealed a significant downward trend in inflammatory factors and liver p38MAPK and NF-κB phosphorylation levels. These results suggest that debridement during the shock period can reduce inflammation through the p38MAPK/NF-κB pathway, promoting a faster decline in systemic inflammatory response.