Abstract
Backgound: Frostbite injury results in serious skeletal muscle damage. Potentially the inflammatory response due to frostbite causes local muscle degeneration. Previous studies have shown that the heat shock proteins (hsp) are able to protect against oxidative stress and inflammation.Results: In the present study we examined the effects of the heat shock protein inducer, 17‐Dimethylaminoethylamino‐17‐demethoxygeldanamycin (17‐DMAG) which was administered within 45 minutes following frostbite injury. Our results show that rat hind‐limb muscles injected with 17‐DMAG following frostbite injury exhibit less inflammatory cell infiltration as compared to control rat hind‐limb muscles. In agreement with this observation, we found that the increased heat shock protein expression results in a decrease in inflammatory cytokine expression. We also found that administration of 17‐DMAG after frostbite injury is able to preserve muscle function. Our results therefore suggest that 17‐DMAG protects skeletal muscle if administered shortly after frostbite injury.Conclusion: We conclude that compounds such as 17‐DMAG that induce heat shock proteins are able to preserve skeletal muscle function and structure if injected within 45 minutes after frostbite injury. Our studies provide the basis for the development of a potential therapeutic strategy to treat injury caused by frostbite.Grant Funding Source: This research was supported by an award from the USAMRMC.
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