Sodium Butyrate Downregulates Implant-Induced Inflammation in Mice

AbstractSodium butyrate (NaBu), a histone deacetylase inhibitor, has shown to exert beneficial actions attenuating inflammation in a number of intestinal and extra-intestinal diseases. However, the effects of NaBu on persistent inflammatory processes as in a response to implantation of foreign material have not been investigated. Synthetic matrix of polyether-polyurethane sponge was implanted in mice ’s subcutaneous layer of the dorsal region, and the animals were treated daily with oral administration of NaBu (100 mg/kg). After 7 days, the implants were removed and processed for assessment of inflammatory markers. Butyrate treatment caused a significant attenuation of neutrophil and macroph age infiltration in implants, which was reflected by the reduction of myeloperoxidase and N-acetyl-β-D-glucosaminidase activities, respectively. Similar reduction was observed in intra-implants nitrite levels of NaBu-treated mice. NaBu treatment was also able to decrease mast cell recruitment/activ ation and the levels of CXCL1, CCL2, IL-6, TNF-ɑ, and TGF-β1 in the implants but did not alter the levels of IL-10. In addition, NaBu administration decreased the concentration of proteins p65 and p50 in the nucleus as compared with the cytoplasm by western blot analysis. This result suggests that treatment with NaBu inhibited the NF-κB pathway. The circulating levels of TNF-ɑ and TGF-β1 were also attenuated by NaBu. Persistent inflammation at sites of implanted devices very often imp...
Source: Inflammation - Category: Allergy & Immunology Source Type: research