Study on the mechanism of the Pu-erh tea (Camellia sinensis var. assamica) extract inhibiting contraction of isolated mouse duodenum

Abstract

The aims of this study were to investigate the effects of three different concentrations of the Pu-erh tea extract (PTE) on the contractile activity of the isolated mouse duodenum and explore their mechanism. The contraction amplitude and frequency of the isolated mouse duodenum were inhibited by all three concentrations of PTE. The high-concentration PTE significantly (P < 0.01) inhibited the promotion effects of acetylcholine chloride or BayK8644 on the amplitude and frequency of intestinal contraction, which were comparable to those of atropine sulphate and verapamil hydrochloride, respectively. The results of UV-Vis and ELISA showed that the content of methionine-enkephalin (Met-ENK) in the PTE-treated groups was decreased to varying degrees; contrarily, the activities of tyrosine hydroxylase (TH), total nitric oxide synthase, and the content of nitric oxide were increased to different degrees. The results suggest that PTE can inhibit the contraction of the isolated mouse duodenum, and the mechanism of action is that PTE can not only inhibit the signal transduction pathways of AC-cAMP-PKA and PLC-IP3-Ca2+, but also the Ca2+ signal systems mediated by G protein-coupled M receptors through the myenteric plexus. By reducing the release of Met-ENK from the motor neurons of the myenteric plexus, the GTP-cAMP-PKK signalling pathway and the Ca2+ signalling system mediated by G protein-coupled delta receptors were inhibited. By increasing the TH activity of the motor neurons in the myenteric plexus, the norepinephrine content was increased, thereby the AC-cAMP-PKA signal transduction pathway mediated by G protein-coupled β receptors was activated. This study increases knowledge regarding the medicinal value of the Pu-erh tea.