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Deprecated: Implicit conversion from float 247.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 J+Surg+Res 2013 ; 185 (2): 726-32 Nephropedia Template TP
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Phosphoinositide 3-kinase/Akt pathway is involved in mediating the anti-inflammation effects of magnesium sulfate #MMPMID23859135
Su NY; Peng TC; Tsai PS; Huang CJ
J Surg Res 2013[Dec]; 185 (2): 726-32 PMID23859135show ga
BACKGROUND: We sought to elucidate whether enhancing phosphoinositide 3-kinase (PI3K)/Akt activity is a crucial mechanism underlying the anti-inflammation effects of magnesium sulfate (MgSO4). MATERIALS AND METHODS: Murine macrophages (RAW264.7 cells) were stimulated with endotoxin, endotoxin plus MgSO4, or endotoxin plus MgSO4 plus PI3K inhibitor (LY294002 or wortmannin). Control groups were run simultaneously. After harvesting, we assayed the expression of inflammatory mediators, transcriptional factor nuclear factor kappaB (NF-kappaB), and Akt. RESULTS: MgSO4 significantly attenuated endotoxin-induced upregulation of inflammatory mediators and NF-kappaB, as macrophages treated with endotoxin plus MgSO4 had significantly lower tumor necrosis factor alpha (P = 0.022), macrophage inflammatory protein 2 (P = 0.040), phosphorylated (p)-NF-kappaB p65 (P = 0.003) and p-inhibitor-kappaB (P < 0.001) concentrations as well as lower NF-kappaB DNA binding (P = 0.001) than macrophages treated with endotoxin alone. Moreover, macrophages treated with endotoxin plus MgSO4 plus LY294002 or wortmannin had significantly higher tumor necrosis factor alpha (P = 0.013 and P < 0.001), macrophage inflammatory protein 2 (P = 0.023 and P = 0.003), p-NF-kappaB p65 (P = 0.006 and P < 0.001), and p-inhibitor-kappaB (P = 0.001 and P < 0.001) concentrations, as well as higher NF-kappaB DNA binding (P = 0.038 and P = 0.009), than macrophages treated with endotoxin plus MgSO4, suggesting that PI3K inhibitors reversed these effects of MgSO4. In contrast, macrophages treated with endotoxin plus MgSO4 had significantly higher p-Akt concentration than macrophages treated with endotoxin alone (P = 0.004). Moreover, macrophages treated with endotoxin plus MgSO4 also had significantly higher p-Akt concentration than macrophages treated with endotoxin plus MgSO4 plus LY294002 or wortmannin (P = 0.004 and P < 0.001). CONCLUSIONS: Enhancing PI3K/Akt activity is a crucial mechanism underlying the anti-inflammation effects of MgSO4.
J+Surg+Res 2013 ; 185 (2): 726-32
