Tianjin Medical Journal ›› 2018, Vol. 46 ›› Issue (6): 581-584.doi: 10.11958/20180398

Previous Articles     Next Articles

The role of PI3K/AKT in acute kidney injury induced by abdominal sepsis in rats

YANG Rui, XU Hua, WANG Bing, WANG Yong-qiang   

  1. 1 The First Center Clinical College, Tianjin Medical University, Tianjin 300070, China; 2 Department of Critical Care Medicine, Tianjin First Center Hospital, Tianjin Institute of Emergency Medicine
  • Received:2018-03-16 Revised:2018-04-27 Published:2018-06-15 Online:2018-07-05
  • Contact: WANG Yongqiang E-mail:yongqiangwang1962@sina.com

Abstract: Objective To investigate the role of PI3K/AKT in acute kidney injury (AKI) induced by abdominal sepsis in rat model. Methods The cecal ligation and puncture (CLP) was used to establish rat model of abdominal sepsis. The serum levels of creatinine (Cr) and urea nitrogen (BUN) were detected by automatic biochemical analyzer at different time points (24, 48 and 72 h) after operation. The expressions of PI3K/AKT mRNA were detected by real-time PCR. Western blot assay was used to verify the expression levels of NLRP3, ASC and Caspase-1. The serum levels of TNF-α, IL-1β and IL-18 were detected by enzyme-linked immunosorbent assay. Results The serum levels of Cr and BUN were increased significantly in CLP group compared with those of control group (P<0.05). The expression levels of PI3K/AKT in kidney were significantly increased in rats with abdominal sepsis (P<0.01). And the released NLRP3 inflammasome, which was activated by PI3K / AKT, was significantly increased (P<0.01). Meanwhile, compared with the sham-operated group, the serum levels of IL-1β, TNF - α and IL-18 were increased significantly (P<0.01). Conclusion PI3K / AKT signaling pathway plays an important role in acute kidney injury induced by abdominal sepsis, which activates the NLRP3 inflammasome, increases the release of inflammatory cytokine and aggravates the sepsis condition.

Key words: sepsis, 1-phosphatidylinositol 3-kinase, protein kinases, caspase 1, interleukin-18, acute kidney injury, NLRP3