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Clin Exp Pharmacol Physiol. 2017 Jul;44(7):803-814. doi: 10.1111/1440-1681.12769.

Anti-inflammatory and retinal protective effects of capsaicin on ischaemia-induced injuries through the release of endogenous somatostatin.

Author information

1
Henan University School of Medicine, Kaifeng, China.
2
The First Affiliated Hospital of Henan University, Kaifeng, China.

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 (0.5 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

PMID:
28429852
DOI:
10.1111/1440-1681.12769
[Indexed for MEDLINE]

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