云南民族大学学报(自然科学版)

为探讨增液承气汤加减方对慢性传输型便秘（STC）大鼠的治疗作用及其潜在分子机制，重点分析其对水通道蛋白AQP3、AQP9表达的调控.采用复方地芬诺酯片灌胃建立STC大鼠模型，84只SD大鼠随机分为正常组、模型组、增液承气汤加减方低（9.72 g/kg/d）、中（19.44 g/kg/d）、高（38.88 g/kg/d）剂量组、阳性药组（伊托必利13.5 mg/kg/d）及增液承气汤加减方高剂量+U0126(0.1 mg/kg/d)组，连续干预14 d.结果显示，增液承气汤加减方中、高剂量组及联合组可显著增加粪便数量及含水量（P <0.05），缩短首粒黑便排出时间，提高肠道推进率，并改善结肠肌电活动（频率增加，振幅降低）.分子机制研究表明，增液承气汤加减方能抑制MAPK/ERK信号通路，下调AQP3表达，同时上调AQP9表达（P <0.05），且高剂量组疗效与阳性药相当（P> 0.05）.综上，增液承气汤加减方可能通过调控MAPK/ERK-AQP3/AQP9通路，改善STC大鼠肠道传输功能，为临床治疗提供实验依据.

To investigate the therapeutic effects of Zengye Chengqi Decoction on chronic transit-type constipation(STC) in rats and its underlying molecular mechanisms, particular attention was paid to the regulation of water channel protein expression, specifically AQP3 and AQP9. An STC rat model was established via intragastric administration of Compound Diphenoxylate Tablets. Eighty-four SD rats were randomly assigned to seven groups:normal control, model control, low-dose Zengye Chengqi Decoction(9.72 g/kg/d), medium-dose Zengye Chengqi Decoction(19.44 g/kg/d), high-dose Zengye Chengqi Decoction(38.88 g/kg/d), positive drug control(Itopride 13.5 mg/kg/d), and a combination group receiving high-dose Zengye Chengqi Decoction plus U0126(0.1 mg/kg/d). The intervention lasted for 14 days. Results demonstrated that the medium-and high-dose Zengli Chengqi Decoction groups, as well as the combination group, significantly increased fecal output and water content(P < 0.05),shortened the time to first black stool excretion, enhanced intestinal propulsion rates, and improved colonic myoelectric activity(increased frequency and reduced amplitude). Molecular mechanism studies revealed that Zengye Chengqi Decoction inhibits the MAPK/ERK signaling pathway, downregulates AQP3 expression, and upregulates AQP9 expression(P < 0.05). Notably, the efficacy of the high-dose Zengye Chengqi Decoction group was comparable to that of the positive drug group(P > 0.05). In conclusion, Zengye Chengqi Decoction may improve intestinal transmission function in STC rats by modulating the MAPK/ERK-AQP3/AQP9 pathway, providing a potential experimental basis for clinical applications.