Prevention of inflammatory damage in hypothalamus by supplementation with w3 fatty acid in a sepsis model: the role of the cholinergic receptor
The cholinergic anti-inflammatory pathway has been studied in relation to its immunomodulatory function and effects on infectious processes, including sepsis. Studies from our laboratory suggest the damage of the cholinergic anti-inflammatory response in animals fed with short term HFD. Omega3 polyu...
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| Main Authors: | , , , , , , |
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| Format: | Online |
| Language: | Portuguese |
| Published: |
Universidade Estadual de Campinas
2019
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| Subjects: | |
| Online Access: | https://econtents.sbu.unicamp.br/eventos/index.php/pibic/article/view/2353 |
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| Summary: | The cholinergic anti-inflammatory pathway has been studied in relation to its immunomodulatory function and effects on infectious processes, including sepsis. Studies from our laboratory suggest the damage of the cholinergic anti-inflammatory response in animals fed with short term HFD. Omega3 polyunsaturated fatty acids have an important anti-inflammatory role through the interaction with GPR-120 type receptors. To evaluate if the supplementation with w3 fatty acid prevents inflammatory damage in the hypothalamus in a model of sepsis, swiss male mice were randomly assigned to be fed with normal chow diet (SC) or high fat diet (HFD) for 3 days or orally supplemented during 17 days with w3 fatty acid and fed with HFD for the last 3 days (HFDw3). Sepsis was induced by surgery of cecal ligation and puncture (CLP). At baseline, w3 supplementation was not able to reverse the decrease of the protein content of the ?7 nicotinic acetylcholine receptor (?7nAChR) caused by HFD in the hypothalamus. After CLP surgery, mice that received w3 fatty acid supplementation prior to short term HFD showed increased protein content of ?7nAChR in the hypothalamus and increased survival rate compared to mice fed only with HFD. These results show that the supplementation with w3 fatty acid may be able to prevent damage in a model of sepsis. |
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| ISSN: | 2596-1969 |
