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Regulatory Roles of the PI3K/Akt Signaling Pathway in Rats with Severe Acute Pancreatitis

机译:PI3K / Akt信号通路在重症急性胰腺炎大鼠中的调节作用

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摘要

The phosphatidylinositol 3-kinase(PI3K)/protein kinase B (Akt) pathway plays a key role in inflammation. However, the regulatory roles of PI3K/Akt in severe acute pancreatitis (SAP) have not been elucidated. The aim of this study was to investigate the impact of wortmannin, a PI3K/Akt inhibitor, on SAP rats through exposure to sodium taurocholate (STC) after 3 h and 6 h. The SAP group was found to have a significant increase in pancreas Akt expression, along with the activation of serum amylase, TNF-α, IL-1β, and IL-6, and pancreas histological aggravation. The administration of wortmannin in SAP rats reduced Akt expression, attenuated the level of serum amylase and inflammation factor, and alleviated the damage of pancreatic tissue. Furthermore, the administration of wortmannin led to an obvious reduction in NF-κB and p38MAPK expression in SAP rats. These findings showed that the PI3K/Akt inhibitor wortmannin decreases inflammatory cytokines in SAP rats and suggests its regulatory mechanisms may occur through the suppression on NF-κB and p38MAPK activity.
机译:磷脂酰肌醇3-激酶(PI3K)/蛋白激酶B(Akt)通路在炎症中起关键作用。但是,PI3K / Akt在严重急性胰腺炎(SAP)中的调节作用尚未阐明。这项研究的目的是通过在3小时和6小时后暴露于牛磺胆酸钠(STC)中来研究PI3K / Akt抑制剂渥曼青霉素对SAP大鼠的影响。发现SAP组与血清淀粉酶,TNF-α,IL-1β和IL-6的活化以​​及胰腺组织学恶化相比,胰腺Akt表达显着增加。在SAP大鼠中服用渥曼青霉素可降低Akt表达,减弱血清淀粉酶和炎症因子的水平,并减轻胰腺组织的损伤。此外,渥曼青霉素的给药导致SAP大鼠中NF-κB和p38MAPK表达的明显降低。这些发现表明,PI3K / Akt抑制剂渥曼青霉素可降低SAP大鼠的炎性细胞因子,并表明其调节机制可能通过抑制NF-κB和p38MAPK活性而发生。

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