Spasmolytic effects of aphanizomenon flos aquae (Afa) extract on the human colon contractility

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 β‐PEA, a trace‐amine considered a neuromodulator in the central nervous sys-tem. To date, it is not clear if β‐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 β‐PEA involvement. The organ bath technique, RT‐PCR, and immunohistochemistry (IHC) were used. Klamin® reduced, in a concentra-tion‐dependent manner, the amplitude of the spontaneous contractions. EPPTB, a trace‐amine receptor (TAAR1) antagonist, significantly antagonized the inhibitory effects of both Klamin® and exogenous β‐PEA, suggesting a trace‐amine involvement in the Klamin® effects. Accordingly, AphaMax®, an AFA extract containing lesser amount of β‐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 antag-onist, 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 experi-ments showed that 5‐HT‐positive neurons are co‐expressed with TAAR1 positive neurons. In con-clusion, the results of this study suggest that Klamin® exerts spasmolytic effects in human colon contractility through β‐PEA, that, by activating neural TAAR1, induce serotonin release from sero-toninergic neurons of the myenteric plexus.