Omega-3 Supplementation Prevents Short-Term High-Fat Diet Effects on the α7 Nicotinic Cholinergic Receptor Expression and Inflammatory Response.
Omega-3 Supplementation Prevents Short-Term High-Fat Diet Effects on the α7 Nicotinic Cholinergic Receptor Expression and Inflammatory Response.
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DOI:
10.1155/2021/5526940
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发表时间:
2021
影响因子:
4.6
通讯作者:
Torsoni MA
中科院分区:
文献类型:
--
作者:
Martins ICA;Contieri LS;Amaral CL;Costa SO;Souza ACP;Ignacio-Souza LM;Milanski M;Torsoni AS;Torsoni MA
The study is aimed at investigating if PUFA supplementation could prevent the effects of a short-term HFD on α7nAChR expression and on the severity of sepsis. Swiss mice were used for the in vivo experiments. For the in vitro experiments, we used a microglia cell line (BV-2) and a hepatoma cell line (Hepa-1c1c7) derived from mice. The animals were either fed standard chow, fed a short-term HFD (60%), or given supplementation with omega-3 fatty acid (2 g/kg or 4 g/kg bw) for 17 days, followed by a short-term HFD. Endotoxemia was induced with an intraperitoneal (i.p.) lipopolysaccharide injection (LPS, 5 or 12 mg/kg), and sepsis was induced by subjecting the animals to cecal ligation and puncture (CLP). BV-2 and Hepa-1c1c7 cells were treated with LPS (100 and 500 ng/mL, respectively) for 3 hours. RT-PCR or Western blotting was used to evaluate α7nAChR expression, inflammatory markers, DNMT1, and overall ubiquitination. LPS and HFD reduced the expression of α7nAChR and increased the expression of inflammatory markers. Omega-3 partially prevented the damage caused by the HFD to the expression of α7nAChR in the bone marrow and hypothalamus, decreased the inflammatory markers, and reduced susceptibility to sepsis-induced death. Exposing the BV-2 cells to LPS increased the protein content of DNMT1 and the overall ubiquitination and reduced the expression of α7nAChR. The inflammation induced by LPS in the BV-2 cell decreased α7nAChR expression and concomitantly increased DNMT1 expression and the ubiquitinated protein levels, indicating the participation of pre- and posttranscriptional mechanisms.
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影响因子:
9.3
作者:
O'Mahoney LL;Matu J;Price OJ;Birch KM;Ajjan RA;Farrar D;Tapp R;West DJ;Deighton K;Campbell MD
通讯作者:
Campbell MD
影响因子:
9.3
作者:
Pintado C;Gavilán MP;Gavilán E;García-Cuervo L;Gutiérrez A;Vitorica J;Castaño A;Ríos RM;Ruano D
通讯作者:
Ruano D
影响因子:
5.6
作者:
De Boer, Anna A.;Monk, Jennifer M.;Robinson, Lindsay E.
通讯作者:
Robinson, Lindsay E.
影响因子:
3.1
作者:
Canastar, Andrew;Logel, Judith;Leonard, Sherry
通讯作者:
Leonard, Sherry
影响因子:
7.3
作者:
Parras Souza, Anelise Cristina;Souza, Camilla Mendes;Torsoni, Marcio Alberto
通讯作者:
Torsoni, Marcio Alberto