Autophagy can alleviate severe burn-induced damage to the intestinal tract in mice.

Abstract

BACKGROUND:

The present study was designed to examine the effect of autophagy and apoptosis on intestinal injury in mice after severe burns.

METHODS:

Kunming mice were subjected to third degree burns over 30% of the total body surface area. Damage to the intestine was assessed by examining changes in intestinal mucosal morphology, enzyme-linked immunosorbent assay of serum d-lactate, diamine oxidase, lipopolysaccharide, interleukin-6, and tumor necrosis factor α (marker of intestinal damage), hematoxylin and eosin staining, and Western blotting under 4 experimental conditions: control group, burn only (burn group), burn and administration of rapamycin to stimulate intestinal autophagy (rapamycin group), or burn and administration of 3-methyladenine to inhibit intestinal autophagy (3-methyladenine group).

RESULTS:

At day 1 postburn, the expression levels of light chain 3 II, beclin-1, and cleaved caspase-3 were significantly greater in all 3 groups of mice subjected to the burn injury than in the control group 1 day postburn; while the levels of light chain 3 II and beclin-1 were significantly greater and those of cleaved caspase-3 were significantly less in the rapamycin group than in the burn group. In contrast, light chain 3 II and beclin-1 levels were significantly less and those of cleaved caspase-3 significantly greater in the 3-methyladenine group. All 3 groups subjected to burn injury showed significantly increased levels of d-lactate, diamine oxidase, lipopolysaccharide, interleukin-6, and tumor necrosis factor α. Of the 3 groups, the rapamycin group exhibited the least observed levels, the 3-methyladenine group the greatest, and the burn group intermediate. Pathologic sections of the intestinal tissue showed that all 3 burn groups exhibited severe intestinal mucosal damage at 1 day postburn. The condition of the 3-methyladenine treatment group was worse than that of the rapamycin treatment group, but better than that of the burn group.

CONCLUSION:

Intestinal autophagy is activated in response to intestinal apoptosis after severe burns and may alleviate burn-induced intestinal injury.

• Authors: Duanyang Zhang, Wei Qiu, Peng Wang, Pan Zhang, Fang Zhang, PeiP Wang, Yong Sun
• Journal: Surgery (Surgery) Vol. 162 Issue 2 Pg. 408-417 (08 2017) ISSN: 1532-7361 [Electronic] United States
• PMID: 28624177 (Publication Type: Journal Article)
• Copyright: Copyright © 2017 Elsevier Inc. All rights reserved.

Chemical References

• Interleukin-6
• Tumor Necrosis Factor-alpha
• 3-methyladenine
• Adenine
• Sirolimus

Topics

• Adenine (analogs & derivatives)
• Animals
• Autophagy
• Burns (pathology)
• Disease Models, Animal
• Female
• Interleukin-6 (metabolism)
• Intestinal Mucosa (metabolism)
• Intestines (pathology)
• Male
• Mice
• Sirolimus
• Tumor Necrosis Factor-alpha (metabolism)