Application of vascular endothelial growth factor at different phases of intestinal ischemia/reperfusion: What are its effects on oxidative stress, inflammation and telomerase activity?

BACKGROUND

Intestinal ischemic reperfusion injury (IRI) represents a great challenge in clinical practice, with high morbidity and mortality. Vascular endothelial growth factor (VEGF), as a signal protein, contributes to vasculogenesis and angiogenesis.

OBJECTIVES

To evaluate the local effectiveness of VEGF following intestinal IRI and its relation with application time.

MATERIAL AND

METHODS

Thirty Wistar albino rats were allocated to 5 groups and underwent laparotomy. The superior mesenteric arteries (SMA) were dissected in 4 groups, while the control group (Gr C) underwent a resection of small and large intestines. The VEGF group (Gr V) received VEGF following SMA dissection, with no further intervention, and the remaining 3 groups were subjected to ischemia for 90 min through occlusion of SMA and reperfusion for 4 h. Ischemic reperfusion group (Gr I/R) received no additional medication, while the remaining 2 groups received VEGF just before ischemia (Gr V+I/R) and during reperfusion (Gr I/R+V).

RESULTS

Both applications of VEGF caused decreases in plasma levels of interleukin 6 (IL-6), tumor necrosis factor α (TNF-α), intestinal malondialdehyde (MDA), oxidized glutathione, protein carbonyl levels, and increases in intestinal total glutathione and superoxide dismutase (SOD) levels. Telomerase activity, which disappeared for Gr I/R, was found to be elevated following both treatment groups. Similarly, the histopathological scores were found better for both treatment groups, but Gr V-I/R represented best outcomes.

CONCLUSIONS

The findings of our study revealed that VEGF, applied either before ischemia or during reperfusion, is effective on local damage following intestinal IRI. By interpreting the biochemical analysis and histopathological findings, we conclude either treatment option to be considered according to the reason of intestinal IRI.