Gastro protective properties of the novel prostone SPI-8811 against acid-injured porcine mucosa

Figure 1 Barrier function of acid injured porcine gastric mucosa to pretreatment of SPI-8811 (1 μmol/L). A: Porcine gastric mucosa mounted on Ussing chambers challenged with mucosal acid (HCl, pH 1.5) over a 90 min period had significantly lower transepithelial electrical resistance (TER) (100 Ω.cm²vs 50 Ω.cm²) when compared with control tissues bathed in normal Ringer’s (NR). Mucosal application of the ClC-2 agonist SPI-8811 (1 μmol/L) prior to application of acid blocked reductions in TER (TER, 50 Ω.cm²vs 100 Ω.cm²) .Values represent means ± SE, n = 8, ^bP < 0.01 vs all other treatment groups; B: As an alternative assessment of gastric mucosal barrier function, mucosal-to-serosal fluxes of ³H-mannitol were examined. In agreement with TER responses, ³H-mannitol flux was significantly elevated by treatment with acid (³H-mannitol flux, 0.02 μmol/L.cm²vs 0.10 μmol/L.cm²), and this response was inhibited by SPI-8811. (³H-mannitol flux, 0.10 μmol/L.cm²vs 0.04 μmol/L.cm²). Values represent mean ± SE, n = 6, ^bP < 0.01 vs all other treatment groups.