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This study was designed to investigate the effect of Aurantii fructus immaturus flavonoid (AFIF) on the contraction of isolated gastric smooth muscle in rats and explore its underlying mechanisms. Isolated antral longitudinal smooth muscle strip (ALSMS) and pyloric circular smooth muscle strip (PCSMS) of rats were suspended in tissue chambers. The responses of ALSMS and PCSMS to administration of AFIF were observed. Cyclic guanosine monophosphate (cGMP) and protein kinase G (PKG) levels of PCSMS were measured by ELISA kits. In this study, AFIF showed no significant effect on ALSMS contraction, but it dose-dependently reduced the mean contraction amplitude of PCSMS. When the concentration of AFIF reached 3000 μg/mL, 6000 μg/mL, and 10000 μg/mL, its inhibitory effect on PCSMS contraction was significant. This effect of AFIF was weakened in Ca2+-rich environment. And Nω-nitro-L-arginine methyl (L-NAME), the inhibitor of nitric oxide synthase (NOS), significantly inhibited AFIF’s action in comparison with control (P<0.05). After incubation with AFIF for 30 min, levels of cGMP and PKG in PCSMS were significantly increased compared with control (P<0.05). Our results suggest that AFIF has a dose-dependent diastolic effect on PCSMS in rats, which may be related to the regulatory pathway of NO/cGMP/PKG/Ca2+. [ABSTRACT FROM AUTHOR]

TongXie-YaoFang (TXYF) can effectively alleviate the symptoms of diarrhea-predominant irritable bowel syndrome (D-IBS) patients. However, the curative mechanism has not been fully clarified. The study was designed to investigate the effect of TXYF on the colonic ion transport induced by serotonin (5-HT) in D-IBS rats. A method of multiple stress (neonatal maternal separation (NMS) combined with restraint stress (RS)) was used to induce the D-IBS model. The model rats were randomly divided into two groups: NMS + RS group and TXYF-formula group, and the normal control (no handling) rats were classified as NH group. In the NMS + RS group, the change of short-circuit current (ΔIsc) induced by 5-HT was lower than that in the NH and TXYF-formula groups. After removing of the extracellular Cl− or HCO3- or basolateral Na+ or blocking the cystic fibrosis transmembrane conductance regulator (CFTR), Na+-K+-2Cl− cotransporter (NKCC), Na+-HCO3- cotransporter, Cl-/HCO3- exchanger, K+ channel, or Na+/K+-ATPase, respectively, there was no difference in 5-HT-induced ΔIsc among the three groups. These data suggest that TXYF can regulate 5-HT-induced Cl− and HCO3- secretion, possibly mediated by the combined action of CFTR, NKCC, Na+-HCO3- cotransporter, Cl-/HCO3- exchanger, K+ channel, and Na+/K+-ATPase. [ABSTRACT FROM AUTHOR]