Ischemic preconditioning and the gene expression of enteric endothelial cell biology of rats submitted to intestinal ischemia and reperfusion

Abstract

PURPOSE:To investigate the effects of ischemic preconditioning (IPC) on the expression of pro and anti-apoptotic genes in rat endothelial cells undergoing enteric ischemia (I) and reperfusion (R). METHODS:Thirty rats underwent clamping of the superior mesenteric vessels. Sham group (GS) laparotomy only; Ischemia (GI):intestinal ischemia (60 min); Ischemia and Reperfusion (GIR): ischemia (60 min) and reperfusion (120 min); Ischemia and intestinal ischemic preconditioning (GI + IPC) : 5 minutes of ischemia followed by 10 min of reperfusion before sustained ischemia (60 min) ischemia and reperfusion and IPC (GIR + IPC): 5 min ischemia followed by 10 min of reperfusion before sustained ischemia (60min) and reperfusion (120 min). Rat Endothelial Cell Biology (PCR array) to determine the expression of genes related to endothelial cell biology. RESULTS:Gene expression of pro-apoptotic markers (Casp1, Casp6, Cflar, Fas, and Pgl) was down regulated in GI+IPC and in GIR + IPC. In contrast, the expression of anti-apoptotic genes (Bcl2 and Naip2), was up-regulated in GI + IPC and in GIR + IPC. CONCLUSION:Ischemic preconditioning may protect against cell death caused by ischemia and reperfusion.

The role of ischemic preconditioning in gene expression related to inflammation in a rat model of intestinal ischemia-reperfusion injury

“…Acta Cir Bras. 2018;33(12):1095-1102 treatments [14][15][16] . By using Rat Endothelial Cell Biology PCR microarray, we investigate if intestinal I/R modifies gene expression encoding proinflammatory proteins in the rat enteric endothelial cells and if IPC treatment modifies this response.…”

The role of ischemic preconditioning in the expression of apoptosis-related genes in a rat model of intestinal ischemia-reperfusion injury

“…For instance, Bax protein forms a heterodimer with Bcl2, which activates the apoptotic pathway. Bax increases the opening of the mitochondrial voltage-dependent anion channel (VDAC), leading to a loss in membrane potential and release of cytochrome “c” to the cytoplasm, thus activating the apoptotic cascade 16 . In our study, Bax was not down regulated in the groups subjected to IPC, suggesting that IPC stimulus is unable to interfere with Bax gene expression in our experimental conditions.…”

“…The cystein-aspartic acid protease (caspase) family is involved in the signal transduction pathways of apoptosis, necrosis and inflammation 16 . There are two families of caspases: the inflammatory caspases and the apoptotic caspases, and each of these families can be further classified into initiator and effector subgroups.…”

“…Effector caspases (caspases 3, 6, and 7) are responsible for cleaving downstream substrates and are sometimes referred to as executioner caspases. Caspase 3 cleaves and activates caspases 6, 7 and 9, whereas caspase 3 itself is processed by caspases 8, 9 and 10 16 .…”

“…This cytokine is produced by activated macrophages as a proprotein, which is proteolytically converted into its active form by caspase 1 (CASP1/ICE). IL1- β is an important mediator of the inflammatory response and is involved in several cellular activities such as cell proliferation, differentiation, and apoptosis, as well as septic shock and wound healing 16 , 19 .…”