目的观察匹维溴胺对腹泻型肠易激综合征(D-IBS)模型大鼠血清以及结肠组织血管活性肠肽(vasoactiveintestinal peptide,VIP)含量、结肠组织水通道蛋白3(aquaporin 3,AQP3)表达的影响,探讨其治疗D-IBS的作用机制。方法采用慢性应激与束缚相结合方法建立D-IBS大鼠模型。采用ELISA法检测VIP含量;采用Real time-PCR法和SABC免疫组化法检测AQP3的表达。结果在血清和结肠组织中VIP的含量,与对照组[(3.092±0.613)ng/ml,(3.811±0.275)ng/ml]比较,模型组[(10.460±1.666)ng/ml,(4.495±0.341)ng/ml]与匹维溴胺组[(5.639±1.163)ng/ml,(4.063±0.534)ng/ml]均升高(P<0.05),尤以模型组升高的更为明显(P<0.01);两组AQP3的表达均下调(P<0.01),尤以模型组AQP3蛋白表达下调显著。结论匹维溴胺治疗D-IBS的作用机制之一,可能与抑制结肠组织中VIP分泌和上调AQP3表达有关。 Objective To observe the effect of pirfenidium bromide on serum and vasoactive intestinal peptide (VIP) and the expression of aquaporin 3 (AQP3) in colon tissue of diarrhea-predominant irritable bowel syndrome (D-IBS) Expression of the impact of its treatment of D-IBS mechanism of action. Methods D-IBS rat model was established by a combination of chronic stress and restraint. The content of VIP was detected by ELISA. The expression of AQP3 was detected by Real time-PCR and SABC immunohistochemistry. Results Compared with the control group [(3.092 ± 0.613) ng / ml, (3.811 ± 0.275) ng / ml], the levels of VIP in serum and colon tissue were significantly lower in model group [(10.460 ± 1.666) ng / ml and 0.341) ng / ml] and pirfenidone group [(5.639 ± 1.163) ng / ml, (4.063 ± 0.534) ng / ml], especially in the model group (P <0.01). The expression of AQP3 was down-regulated in both groups (P <0.01), especially in model group. Conclusions Pivoxil treatment of D-IBS one of the mechanisms may be related to the inhibition of VIP secretion in colon tissue and up-regulated AQP3 expression.