AIM:This investigation was to reveal the characteristics andmechanism of enzyme secretion and increase in [Ca~(2+)]_istimulated by seikoeaponin(I)[SA(I)]in rat pancreatic acini.METHODS:Pancreatic acini were prepared from male Wistarrats.Isolated acinar cells were suspended in Eagle’s MEMsolution.After adding drugs,the incubation was performedat 37℃ for a set period of time.Amylase of supernatant wasassayed using starch-iodide reaction.Isolated acinar singlecell was incubated with Fura-2/AM at 37℃,then cells werewashed and resuspended in fresh solution and attached tothe chamber.Cytoplasm [Ca~(2+)]_i of a single cell wasexpressed by fluorescence ratio F340/F380 recorded in aNikon PI Ca~(2+)measurement system.RESULTS:Rate course of amylase secretion stimulated bySA(I)in rat pancreatic acini appeared in ball-like shape.Thepeak amplitude increased depended on SA(I)concentration.The maximum rate responded to 1×10~5 mol/L SA(I)was 13.l-fold of basal and the rate decreased to basel level at 30min.CCK-8 receptor antagonist Bt_2-cGMP markedly inhibitedamylase secretion stimulated by SA(I)and the dose-effectrelationship was similar to that by CCK-8.[Ca~(2+)]_i in a singleacinar cell rose to the peak at 5 min after adding 5×10~(-6)mol/LSA(I)and was 5.1-fold of basal level.In addition,there was asecondary increase after the initial peak.GDP could inhibitboth the rate of amylase secretion and dsing of [Ca~(2+)]_istimulated by SA(I)in a single pancreatic acinar cell.CONCLUSION:SA(I)is highly efficient in promoting thesecretion of enzymes synthesized in rat pancreatic acini andraising intrecellular [ Ca~(2+)]_i.Signaling trensduction pathwayof SA(I)involves activating special membrane receptor andincrease in cytoplasm [Ca~(2+)]_i sequentially. AIM: This investigation was to reveal the characteristics and mechanism of enzyme secretion and increase in [Ca ~ (2 +)] _ istimulated by seikoeaponin (I) [SA (I)] in rat pancreatic acini.METHODS: Pancreatic acini were prepared from male Wistarrats . Isolated acinar cells were suspended in Eagle’s MEMsolution. After adding drugs, the incubation was performed at 37 ° C for a set period of time. Amylase of supernatant wasassayed using starch-iodide reaction. Isolated acinar single cells were incubated with Fura-2 / AM at 37 ℃, then cells were washed and resuspended in fresh solution and attached to the reaction chamber. Cytoplasm [Ca ~ (2 +)] _i of a single cell wasexpressed by fluorescence ratio F340 / F380 recorded in aNikon PI Ca ~ (2+) measurement system .RESULTS : Rate course of amylase secretion stimulated by SA (I) in rat pancreatic acini was in ball-like shape. The peak amplitude increased at SA (I) concentration.The maximum rate responded to 1 × 10 -5 mol / L SA (I) was 13.l-fold of basal and the rate decreased to basel level at 30min.CCK-8 receptor antagonist Bt_2-cGMP markedly inhibited amylase secretion stimulated by SA (I) and the dose-effect relationship was similar to that by CCK-8. [Ca ~ (2 +)] _i in a single cell nucleus rose to the peak at 5 min after adding 5 × 10 -6 mol / LSA (I) and was 5.1-fold of basal level. In addition, there was a second increase after the initial peak. GDP could inhibit the rate of amylase secretion and dsing of [Ca ~ (2 +)] _ istimulated by SA (I) in a single pancreatic acinar cell. CONCLUSION: SA (I) is highly efficient in promoting thesecretion of enzymes synthesized in rat pancreatic acini andraising intrecellular [Ca ~ (2+ )] _i.Signaling trensduction pathwayof SA (I) involves activating special membrane receptor and activation in cytoplasm [Ca ~ (2 +)] _i sequentially.