Interleukin-33 Prevents Retinal Ischemia Reperfusion Injury in Rats by Preventing Apoptosis

Background Retinal ischemia reperfusion (RIR) injury is a common pathological process that can result in visual impairment in many ophthalmic diseases. Inflammation and apoptosis play an important role in RIR injury. Objectives This experimental study was designed to explore the ability of a new cytokine, IL-33, to attenuate RIR injury via an apoptosis-inhibitory mechanism. Methods From June, 2015 to October, 2015, 40 Sprague-Dawley (SD) rats from Wuhan university in China were divided into the following four groups: normal control group (NCG), RIR injury model group (MG), IL-33 pretreatment group (IL-33), and PBS group (PBS) according to random number tables. Rats in the IL-33 and PBS groups received an intravitreous injection of 2 μg of recombinant IL-33 (rIL-33) or PBS one hour before the induction of ischemia. Histological evaluation, inflammatory cell infiltration, and apoptosis of retinal cells were examined. The expressions of apoptotic-related proteins (Bcl-2 and Bax) were quantified by immunohistochemistry and western blotting. The presence of NF-κB p65 in the retina was assessed by western blotting. Results Our data revealed that IL-33 pretreatment maintained a better retinal structure, inhibited leukocyte infiltration (IL-33 vs. MG with P < 0.01 and IL-33 vs. PBS group with P < 0.01), and reduced the apoptosis of retinal ganglion cells (IL-33 vs. MG with P < 0.05 and IL-33 vs. PBS group with P < 0.05). Furthermore, IL-33 upregulated the expression of Bcl-2and decreased the expression of Bax (IL-33 vs. MG with P < 0.01 and IL-33 vs. PBS group with P < 0.01). In addition, IL-33 attenuated NF-κB p65 levels in the retina and inhibited the activation of NF-κB (IL-33 vs. MG with P = 0.021 and IL-33 vs. PBS group with P = 0.025). Conclusions IL-33 may be a potential new agent to attenuate RIR injury by reducing inflammatory cell infiltration and preventing apoptosis.