Effect of AVS Retina in a rodent model of retinal ischemia‐reperfusion

Abstract

PurposeAnti‐VEGF agents currently available for the treatment of Diabetic Retinopathy and Wet Age‐Related Macular Degeneration do not possess a direct effect on inflammation. Our previous findings show that a nutritional supplement formula codenamed AVS is able to inhibit nitric oxide and prostaglandin E2 accumulation by modulating important pro‐inflammatory genes in vitro. Here, we set out to test whether AVS may exert a protective effect in a model of retinal ischemia/reperfusion (IR) damage in rat.MethodsBrown Norway rats were subjected to retinal IR injury by rising intraocular pressure to 130 mmHg for 60 minutes. Animals were treated once daily by oral gavage with AVS or vehicle (VHC) starting five days before insult and until sacrifice 6 hours (T6 h) or 7 days (T7) after IR. Electroretinograms (ERG) were recorded in unconscious rats before IR (baseline), and then at T3 and T7. Total RNA was extracted from retinas at T6 h to assess the expression of tumor necrosis factor alpha (TNFa) mRNA by Real‐time RT‐PCR.ResultsRetinal ischemia in VHC and AVS groups produced a significant reduction of a‐ and b‐wave amplitudes at T3 when compared with baseline. Notably, a‐ and b‐wave amplitudes reduction observed at T7 in the VHC group was significantly inhibited (p≤0.05) by treatment with AVS. Moreover, the a‐ and b‐wave amplitudes in the AVS group were found not to differ from baseline (p>0.05) while being markedly suppressed in the VHC‐treated rats (p≤0.05). The expression of TNFa was strongly upregulated in the VHC group as assessed in retinas sampled at T6 h. Most importantly, treatment with AVS significantly reduced TNFa expression compared to VHC (p≤0.05).ConclusionsAVS was found to reduce retinal damage caused by IR favoring its functional recovery possibly by a mechanism involving inhibition of early pro‐inflammatory mediators such as TNFa.