Vascular endothelial injury and apoptosis in rats with severe acute pancreatitis

Abstract

We explored mechanisms of vascular endothelial injury that lead to systemic multiple organ failure by detecting the soluble endothelial protein C receptor (sEPCR), von Willebrand factor (vWF), serum nitric oxide (NO), and tumor necrosis factor alpha (TNF-α) and Bcl-2 mRNA and Bax mRNA expression in a severe acute pancreatitis (SAP) rat model. Compared to controls, the levels of TNF-α, vWF, and sEPCR were significantly increased in the experimental group at 12 hours and 24 hours and the NO level was significantly decreased. After 12 hours, the aortic endothelial apoptosis index and Bax mRNA expression in aortic endothelial cells had increased in the experimental group, but Bcl-2 mRNA levels had decreased. All these changes appeared at both 12 h and 24 hours. The results indicated that vascular endothelial injury and apoptosis markers were elevated in SAP. Endothelial injury and increased apoptosis in the experimental group were related to the increased expression of TNF-α.

Figure 1

Pancreatic tissue HE staining.

Figure 2

(a) BCL-2 and (b) Bax RT-PCR analysis of the aortic endothelium in the experimental and control groups after 12 hours and 24 hours.

Figure 3

Aortic endothelial cell apoptosis TUNEL analysis results. (a), (b) Aortic endothelial cell apoptosis in the control group after 12 h (a) and 24 h (b). (c), (d) Aortic endothelial cell apoptosis in the experimental group after 12 h (c) and 24 h (d).