The Thai Journal of Veterinary Medicine


The objectives of this study were to observe the effect of different concentrations of Fomes officinalis polysaccharides (FOPs) on the contractile activity of the isolated duodenal smooth muscle in mice and explore its mechanism. The contractility of the isolated duodenum was recorded by the Medlab biological signal acquisition and processing system before and after administration and the effects of FOPs-treated groups at low, medium and high dose (5, 10 and 20 mg/mL) on the contractile frequency and amplitude of the intestines were observed. Adrenaline hydrochloride (AD) and CaCl2 were selected respectively to be co-incubated with the high dose FOPs to observe the effects on duodenal contraction. The effects of different concentrations of the FOPs on the activities of acetylcholine transferase (ChAT), acetylcholine Esterase (A-CHE), total nitric oxide synthase (TNOS) and the content of Leucine-enkephalin (Leu-enk) in the isolated duodenum of the myenteric plexus in mice were detected by UV-Vis and enzyme-linked immunosorbent assay (ELISA). The results showed that the three FOPs-treated groups had different inhibitory effects on the contractile frequency and amplitude of the isolated duodenum in mice compared with those before administration. The high dose FOPs could synergize (P<0.01) the inhibition effect of AD on the frequency and amplitude of the intestinal contraction and could significantly (P<0.01) inhibit the promotion effect of CaCl2 on it. The effect was equivalent to that of isoprenaline hydrochloride (ISO) or verapamil hydrochloride, respectively. The results of UV-Vis and ELISA showed that compared with the control group, the activity of ChAT and the content of Leu-enk in the three FOPs-treated groups decreased to varying degrees, contrarily, the activities of A-CHE and TNOS significantly increased (P<0.01). All the results suggest that the FOPs can inhibit the contraction of the isolated duodenum in mice, and the mechanism of action is that the FOPs cannot only inhibit the signal transduction pathways of G protein-coupled M receptor-mediated ACcAMP-PKA and PLC-IP3- Ca2+, but also the Ca2+ signalling systems (such as inhibiting ICa-L of the muscle membrane and then inhibiting Ca2+-CaM signalling pathway) through the myenteric plexus. By inhibiting the release of Leu-enk from the motor neurons of the myenteric plexus, the G protein-coupled delta receptor-mediated GTP-cAMP- (PKK or PKC) signalling pathway and Ca2+ signalling systems were inhibited. By promoting the release of NOS from the motor neurons of the myenteric plexus, the increased NO was induced, then the enzyme-linked receptor-mediated GC-cGMPPKG signal transduction pathway was reactivated. The G protein-coupled receptor-mediated AC-cAMP-PKA signal transduction pathway was activated by the myenteric plexus.

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