Seawater exposure exacerbates scald burns-induced intestinal injury in rabbits:study of the mechanisms
10.3969/j.issn.1673-4254.2014.06.25
- VernacularTitle:兔烫伤合并海水浸泡后加重肠道损伤的机制
- Author:
Pei XU
1
;
Jiahan WANG
;
Pengwei SHI
;
Jun MA
Author Information
1. 南方医科大学南方医院烧伤科
- Keywords:
burn injury;
seawater exposure;
oxygen free radicals;
intestinal injury
- From:
Journal of Southern Medical University
2014;(6):880-884
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the effect of seawater exposure on intestinal injury in rabbits with scald burns and explore the mechanisms. Methods Sixty-three rabbits with scald burns covering 20%total body surface area were randomized equally into scald control group (group A), scald with freshwater exposure group (group B), and scald with seawater exposure group (group C). At 2, 4 and 8 h after scald burns, 7 rabbits from each group were sacrificed for detecting plasma superoxide dismutase (SOD) and lipid peroxide (LPO) levels and intestinal contents of prostaglandins (PGs) and for examining the intestinal pathologies; immunohistochemistry was used to detect the expression of Bax and Bcl-2 proteins in the small intestinal epithelium. Results The rabbits in group C showed severer intestinal mucosal and barrier function damages than those in groups A and B. The plasma SOD activity and intestinal PGs contents were significantly lowered in group C than in groups A and B at 2, 4, and 8 h postburn (P<0.01) and reduced as the postburn time extended (P<0.01). In group C, plasma LPO content was the highest among the groups (P<0.01) and increased significantly with the seawater exposure time (P<0.01). The expression of Bax and Bcl-2 in the intestinal mucosal tissues was also the highest in group C (P<0.01) at 4 h and 8 h postburn and increased significantly with time (P<0.01). Conclusion Seawater exposure exacerbates scald burn-induced intestinal mucosal and barrier function damages in rabbits mainly by aggravating intestinal inflammation and structural damage, as evidenced by decreased intestinal PGs contents and plasma SOD activity, increased plasma PLO content, and enhanced Bax and Bcl-2 protein expressions in the intestinal mucosa.
