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• W1754767791 abstract "Background Hyperglycemia with insulin resistance remains a challenging problem in severely burned patients. Recent studies indicated the involvement of the nucleotide-binding domain and the leucine-rich, repeat-containing family, pyrin-containing 3 (NLRP3) inflammasome in insulin resistance and a beneficial role of apelin in insulin resistance. Our aim was to investigate whether apelin inhibits the activation of the NLRP3 inflammasome and ameliorates insulin resistance in severely burned rats. Methods Male Wistar rats were subjected to a full-thickness burn injury comprising 40% of the total body surface area and were randomized to receive apelin, NG-methyl-L-arginine acetate salt (L-NMMA), and apelin plus treatments with L-NMMA. The following outcome measurements were assessed: apelin/APJ mRNA expression in white adipose tissue (WAT) and muscles, plasma apelin level, and activation of the NLRP3 inflammasome in WAT, Interleukin-1 β, interleukin-6, tumor necrosis factor-α, and monocyte chemoattractant protein-1 levels in plasma, insulin resistance, survival rates, and endothelial nitric oxide synthase phosphorylation in soleus muscles. Results Severe burn induced a decreased expression of apelin/APJ mRNA in soleus muscles and a decrease in plasma apelin levels. Burn injury with apelin treatment restored plasma apelin level, inhibited NLRP3 inflammasome activity in WAT, and decreased inflammatory cytokine levels in plasma. Rats treated with apelin also showed improved insulin sensitivity and decreased mortality, accompanied by a remarkable induction of endothelial nitric oxide synthase phosphorylation in soleus muscle. Furthermore, the aforementioned effects of apelin were inhibited in part by treatment with L-NMMA. Conclusion Apelin inhibits the activation of NLRP3 inflammasome, attenuates systemic inflammatory response, ameliorates insulin resistance, and promotes survival after severe burn, in part through an endothelial nitric oxide synthase–dependent pathway. Hyperglycemia with insulin resistance remains a challenging problem in severely burned patients. Recent studies indicated the involvement of the nucleotide-binding domain and the leucine-rich, repeat-containing family, pyrin-containing 3 (NLRP3) inflammasome in insulin resistance and a beneficial role of apelin in insulin resistance. Our aim was to investigate whether apelin inhibits the activation of the NLRP3 inflammasome and ameliorates insulin resistance in severely burned rats. Male Wistar rats were subjected to a full-thickness burn injury comprising 40% of the total body surface area and were randomized to receive apelin, NG-methyl-L-arginine acetate salt (L-NMMA), and apelin plus treatments with L-NMMA. The following outcome measurements were assessed: apelin/APJ mRNA expression in white adipose tissue (WAT) and muscles, plasma apelin level, and activation of the NLRP3 inflammasome in WAT, Interleukin-1 β, interleukin-6, tumor necrosis factor-α, and monocyte chemoattractant protein-1 levels in plasma, insulin resistance, survival rates, and endothelial nitric oxide synthase phosphorylation in soleus muscles. Severe burn induced a decreased expression of apelin/APJ mRNA in soleus muscles and a decrease in plasma apelin levels. Burn injury with apelin treatment restored plasma apelin level, inhibited NLRP3 inflammasome activity in WAT, and decreased inflammatory cytokine levels in plasma. Rats treated with apelin also showed improved insulin sensitivity and decreased mortality, accompanied by a remarkable induction of endothelial nitric oxide synthase phosphorylation in soleus muscle. Furthermore, the aforementioned effects of apelin were inhibited in part by treatment with L-NMMA. Apelin inhibits the activation of NLRP3 inflammasome, attenuates systemic inflammatory response, ameliorates insulin resistance, and promotes survival after severe burn, in part through an endothelial nitric oxide synthase–dependent pathway." @default.
• W1754767791 created "2016-06-24" @default.
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• W1754767791 date "2015-06-01" @default.
• W1754767791 modified "2023-10-10" @default.
• W1754767791 title "Apelin inhibits the activation of the nucleotide-binding domain and the leucine-rich, repeat-containing family, pyrin-containing 3 (NLRP3) inflammasome and ameliorates insulin resistance in severely burned rats" @default.
• W1754767791 cites W1971203472 @default.
• W1754767791 cites W1974953974 @default.
• W1754767791 cites W1979089779 @default.
• W1754767791 cites W1980717583 @default.
• W1754767791 cites W1983984331 @default.
• W1754767791 cites W1985167082 @default.
• W1754767791 cites W1985471608 @default.
• W1754767791 cites W1988870963 @default.
• W1754767791 cites W1996696087 @default.
• W1754767791 cites W2000379370 @default.
• W1754767791 cites W2009523990 @default.
• W1754767791 cites W2011296046 @default.
• W1754767791 cites W2012461909 @default.
• W1754767791 cites W2023289992 @default.
• W1754767791 cites W2026850406 @default.
• W1754767791 cites W2029920356 @default.
• W1754767791 cites W2030015146 @default.
• W1754767791 cites W2031684439 @default.
• W1754767791 cites W2035942181 @default.
• W1754767791 cites W2036341862 @default.
• W1754767791 cites W2041510403 @default.
• W1754767791 cites W2052230840 @default.
• W1754767791 cites W2075714512 @default.
• W1754767791 cites W2080549540 @default.
• W1754767791 cites W2082858358 @default.
• W1754767791 cites W2088109563 @default.
• W1754767791 cites W2089827757 @default.
• W1754767791 cites W2096979174 @default.
• W1754767791 cites W2104067489 @default.
• W1754767791 cites W2104966898 @default.
• W1754767791 cites W2113511371 @default.
• W1754767791 cites W2114014847 @default.
• W1754767791 cites W2114570899 @default.
• W1754767791 cites W2116563158 @default.
• W1754767791 cites W2124475225 @default.
• W1754767791 cites W2124731208 @default.
• W1754767791 cites W2124848390 @default.
• W1754767791 cites W2128787151 @default.
• W1754767791 cites W2130495917 @default.
• W1754767791 cites W2145306055 @default.
• W1754767791 cites W2145983343 @default.
• W1754767791 cites W2150702412 @default.
• W1754767791 cites W2152377123 @default.
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• W1754767791 cites W2155885188 @default.
• W1754767791 cites W2157495503 @default.
• W1754767791 cites W2169863070 @default.
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• W1754767791 doi "https://doi.org/10.1016/j.surg.2015.01.011" @default.
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