Abstract
To investigate the role of atenolol in the gene expression of caspase 1 (Casp1) and Bcl2L1 on vascular endothelium of rat intestine after ischemia and reperfusion (IR). Eighteen adult male Wistar rats were randomly divided into 3 groups (n=6): SG (Sham group): no clamping of the superior mesenteric artery; IRG: IR plus saline group: IRG+At: IR plus Atenolol group. Rats from IRG and IRG+At were subjected to 60 min of intestinal ischemia and 120 min of reperfusion. Atenolol (2mg/kg) or saline were injected in the femoral vein 5 min before ischemia, 5 min and 55 min after reperfusion. Thereafter, intestinal segments were appropriately removed and processed for Endothelial Cell Biology Rat RT2 Profiler PCR Array. the anti-apoptotic Bcl2L1 gene expression was significantly down-regulated (-1.10) in the IRG and significantly up-regulated in the IRG+At (+14.15). Meanwhile, despite Casp1 gene expression was upregulated in both groups, it was significantly higher in the IRG (+35.06) than the IRG+At (+6.68). Atenolol presents antiapoptotic effects on rat intestine subjected to IR partly by the up-regulation of the anti-apoptotic Bcl2L1 gene expression. Moreover, atenolol can mitigate the pro-apoptotic and pro-inflammatory effects of Casp1 gene on rat intestine after IR.
Highlights
Ischemia/reperfusion (I/R) injury is a frequent phenomenon that is associated to high morbidity and mortality[1,2,3,4]
The rats from IRG and IRG+At were subjected to 60 min of intestinal ischemia followed by 120 min of reperfusion
Despite the apoptotic CASP1 gene expression was up-regulated in both groups, it was significantly (p
Summary
Ischemia/reperfusion (I/R) injury is a frequent phenomenon that is associated to high morbidity and mortality[1,2,3,4]. The reoxygenation may worst cell damage by leading to the formation of reactive oxygen species (ROS), which initiates a complex cascade of events that culminate in additional tissue injury, promoting immediate cell death (necrosis), programed cell death (apoptosis) and alteration of cellular phenotype[5,6,7]. Several drugs, such as beta blockers, have been proposed as modulating agents to minimize I/R injury. Increased ROS production and apoptosis are thought to be mediated by the β1 adrenergic receptors, both in-vitro and in-vivo[8]
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