The mechanisms regarding the retinal protective and anti-inflammatory effects of capsaicin (CAP) remain unclear. Somatostatin is contained in CAP-sensitive sensory neurons, including nerve terminals, from which it can be released by capsaicin. The present study provides a novel neurohumoral regulatory mechanism for CAP-induced-endogenous somatostatin in a retinal ischaemia-reperfusion (I/R) mouse model. CAP (0.5 mg/kg) was injected subcutaneously 5 minutes after I/R. A selective somatostatin-depleting agent, cysteamine, was applied subcutaneously 4 hours before the experiment to examine the effects of endogenous somatostatin. Ischaemia and oxidative stress-induced inflammatory factors (CXCL10, CXCR3 and NF-κB p65) were also examined in the present study. The morphometric evaluation showed that the retinal thickness was increased 24 hours after I/R injury and attenuated 7 days after I/R injury. The number of ganglion cells was reduced 7 days after I/R injury. The application of CAP significantly prevented retinal I/R damage. Cysteamine pretreatment reversed the effects of CAP. Inhibition of CXCL10/CXCR3 and NF-κB (especially in astrocytes and microglia/macrophage) was involved in capsaicin-induced retinal protection through endogenous somatostatin. CAP has anti-inflammatory and neuroprotective effects in ischaemia-induced retinal injuries through endogenous somatostatin. Novel therapeutic remedies for inflammation or neuronal injuries were developed based on the systemic humoral effects related to CAP.
Keywords: capsaicin; ischaemia-reperfusion; retina; somatostatin.
© 2017 John Wiley & Sons Australia, Ltd.