Abstract

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 (0.5mg/kg) was injected subcutaneously 5minutes after I/R. A selective somatostatin-depleting agent, cysteamine, was applied subcutaneously 4hours 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 24hours after I/R injury and attenuated 7days after I/R injury. The number of ganglion cells was reduced 7days 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.

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call

Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.