Objective: To investigate the mechanism of Shugan Jianpi Recipe (SJR) on the ion transportation of diarrhea predominant irritable bowel syndrome (IBS-D) colon mucosa induced by 5-HT.
Methods: Totally 36 male SD rats were randomly divided into three groups, i. e., the normal group, the model group, and the SJR group, 12 in each group. IBS-D Rat model was induced by intracolonic instillation of acetic acid and restraint stress. After successful modeling, normal saline was given to rats in the normal group and the model group, while SJR was given to those in the SJR group by gastrogavage for 14 days. The short circuit current (lsc) technology was used to measure 5-HT induced lsc changes of the colon mucosa under the actions of drugs and specific blocking agents.
Results: There was no difference in basal current (BC), the potential difference (PD), and transmembrane resistance (TR) of the distal colon among the 3 groups (all P > 0.05). The 5-HT induced short circuit current change (delta lsc) was lower in the model group than in the normal group (P < 0.05), and it was higher in the SJR group than in the model group (P < 0.05). When 4,4'-diisothiocyanato-stilbene-2,2'-disulfonic acid (DIDS, 500 micromol/L), an Ca(+)-dependent Cl- channel blocker, was added from the epiphragm of the colonic mucosa, the 5-HT induced delta lsc was lower in the model group than in the normal group (P < 0.05), and it was higher in the SJR group than in the model group (P < 0.05). When Na+ was substituted in the epiphragm solution (Na+ free) or amiloride (100 micromol/L) was added from the epiphragm of the colonic mucosa, an epithelial Na+ channel blocker, the 5-HT induced delta lsc was lower in the model group than in the normal group (P < 0.05), and it was higher in the SJR group than in the model group (P < 0.05).
Conclusions: SJR could affect the transmembrane electrolyte transportation of IBS-D rat induced by 5-HT through regulating the secretion of Cl- and HCO3-. The effects might be achieved by the coordination of apical Cl- channel CFTR, basolateral Na(+)-K+ ATPase, sodium-potassium-chloride cotransporter, sodium-bicarbonate cotransporter, Cl-/HCO3- exchanger, as well as K+ channel.