Spasmolytic Effects of Aphanizomenon Flos Aquae (AFA) Extract on the Human Colon Contractility.
- Autori: Amato A; Terzo S; Marchesa P; Maffongelli A; Martorana M; Scoglio S; Mulè Flavia
- Anno di pubblicazione: 2021
- Tipologia: Articolo in rivista
- OA Link: http://hdl.handle.net/10447/530718
Abstract
The blue-green algae Aphanizomenon flos aquae (AFA), rich in beneficial nutrients, exerts various beneficial effects, acting in different organs including the gut. Klamin® is an AFA extract particularly rich in -PEA, a trace-amine considered a neuromodulator in the central nervous system. To date, it is not clear if -PEA exerts a role in the enteric nervous system. The aims of the present study were to investigate the effects induced by Klamin® on the human distal colon mechanical activity, to analyze the mechanism of action, and to verify a -PEA involvement. The organ bath technique, RT-PCR, and immunohistochemistry (IHC) were used. Klamin® reduced, in a concentration-dependent manner, the amplitude of the spontaneous contractions. EPPTB, a traceamine receptor (TAAR1) antagonist, significantly antagonized the inhibitory effects of both Klamin® and exogenous -PEA, suggesting a trace-amine involvement in the Klamin® effects. Accordingly, AphaMax®, an AFA extract containing lesser amount of -PEA, failed to modify colon contractility. Moreover, the Klamin® effects were abolished by tetrodotoxin, a neural blocker, but not by L-NAME, a nitric oxide-synthase inhibitor. On the contrary methysergide, a serotonin receptor antagonist, significantly antagonized the Klamin® effects, as well as the contractility reduction induced by 5-HT. The RT-PCR analysis revealed TAAR1 gene expression in the colon and the IHC experiments showed that 5-HT-positive neurons are co-expressed with TAAR1 positive neurons. In conclusion, the results of this study suggest that Klamin® exerts spasmolytic effects in human colon contractility through -PEA, that, by activating neural TAAR1, induce serotonin release from serotoninergic neurons of the myenteric plexus.