New Approaches in TransplantationExperimental transplantationOctreotide Ameliorates Renal Ischemia/Reperfusion Injury via Antioxidation and Anti-inflammation

- Octreotide could mitigate renal ischemic/reperfusion injury (IRI) and reduce apoptosis in renal tissues in a mouse model.
- Administration of octreotide inhibits the production of inflammatory cytokines in renal IRI and downregulates the expression of nuclear factor-κB p65.
- Octreotide could upregulate the antioxidative stress capacity in a mouse renal IRI model.
- Nuclear factor erythroid 2-related factor 2/heme oxygenase-1 and NAD(P)H quinone oxidoreductase signaling pathways may be involved in the protective effect induced by octreotide in renal IRI in mice.

Oxidative stress, calcium overload, inflammation, cellular necrosis, and apoptosis are implicated in renal ischemic/reperfusion injury (RIRI). Because octreotide (OCT) is protective in retinal IRI, the effect of OCT on mouse RIRI and the mechanisms involved were investigated. The RIRI model was induced in male C57BL/6 mice, and the mice were then treated with saline or OCT. Serum and kidneys were subjected to periodic acid-Schiff staining, terminal deoxynucleotidyl transferase dUTP nick end labeling assay, enzyme-linked immunosorbent assay, western blotting, and immunohistochemistry. Treatment with OCT restored the renal functions and histologic changes induced by RIRI. The administration of OCT reduced tumor necrosis factor-α and interleukin-6 levels in kidney tissues, protected the kidney from apoptosis, and significantly downregulated the expression of nuclear factor-κB p65. In addition, OCT treatment upregulated the expression of nuclear factor erythroid 2-related factor 2, heme oxygenase-1, and NAD(P)H quinone oxidoreductase 1 and enhanced the renal antioxidant capacity. These results cumulatively indicate that OCT may protect the kidneys against IRI in a mouse model through the regulation of antioxidation and anti-inflammation.