Systemic Administration of Interleukin-10 Attenuates Early Ischemic Response Following Spinal Cord Ischemia Reperfusion Injury in Rats

Abstract

The aim of this experimental study was to investigate the early effects of interleukin-10 (IL-10) and interleukin-1beta antagonist (anti-IL-1beta) against cellular damage, inflammatory reactivity, lipid peroxidation (LPO), and myeloperoxidase (MPO) activity induced by spinal cord ischemia reperfusion injury (IRI). Thirty-two single strain female Albino rats were divided into four groups: control (sham-operated), IRI-alone, IL-10-treated (100 mug/kg), and anti-IL-1beta-treated (1 mg/kg) groups after IRI. IRI was induced by balloon occlusion of the aorta and simultaneous hypovolemia during occlusion. The animals were sacrificed at 24 h. Histopathological and ultrastructural analyses, biochemical studies for determination of LPO and MPO activity and Comet assays (single cell electrophoresis for detecting DNA single strand breaks) were performed in all study groups. Compared with the levels of control (sham-operated) animals, IRI produced a significant increase in the levels of LPO and MPO activity, and prominent tissue damage characterized by leukocyte infiltration, edema and neuronal and glial damage in the affected spinal cord in 24 h. The administration of IL-10 decreased LPO and MPO activity, and suppressed initial inflammatory response in the first 24 h. The effects of anti-IL-1beta were limited to decrease in LPO activity without considerable evidence of cellular preservation. These data suggest that systemic administration of IL-10 attenuates the early ischemic response, and may restrict the tissue damage in the first 24 h after spinal cord ischemia reperfusion injury. Anti-IL-1beta has no considerable effect in this time window. The results of this preliminary study promote further studies with longer time windows on the effects of anti-inflammatory cytokines in spinal cord IRI.