【目的】 观察枳实对慢传输型便秘（STC）小鼠的治疗作用及机制。【方法】 采用盐酸洛哌丁灌胃法构建 STC 小鼠模型。 将造模成功的小鼠随机分为模型组，枳实低、高剂量组和枳实高剂量+Masitinib[酪氨酸激酶受体（c-Kit）抑制剂]组，另设正 常组对照。分组干预后，测定小鼠肠道推进率和6 h排便粒数、粪便含水率，苏木精-伊红（HE）染色法观察结肠组织形态变 化，酶联免疫吸附分析（ELISA）检测结肠组织5-羟色胺（5-HT）、血管活性肠多肽（VIP）、P物质（SP）、一氧化氮（NO）含量及 一氧化氮合酶（NOS）活性，实时荧光定量逆转录聚合酶链反应（qRT-PCR）法检测结肠组织干细胞因子（SCF）和 c-Kit基因表 达，Western Blot 法检测结肠组织水通道蛋白 3（AQP3）、水通道蛋白 8（AQP8）、SCF 和 c-Kit 蛋白表达。【结果】 与正常组比 较，模型组小鼠结肠组织明显损伤，排便粒数和粪便含水率，肠道推进率，结肠组织SP含量、c-Kit和SCF基因和蛋白表达 水平降低，结肠组织 5-HT、VIP、NO 含量和 NOS活性，结肠组织 AQP3和 AQP8蛋白表达水平升高，差异均有统计学意义 （P＜0.05）；与模型组比较，枳实低、高剂量组小鼠结肠组织损伤明显改善，排便粒数和粪便含水率，肠道推进率，结肠组 织SP含量、c-Kit和SCF基因和蛋白表达水平升高，结肠组织5-HT、VIP、NO含量和NOS活性，结肠组织AQP3和AQP8蛋 白表达水平降低，差异均有统计学意义（P＜0.05）；Masitinib可部分逆转枳实对STC小鼠排便的改善作用（P＜0.05）。【结论】 枳 实可提高STC小鼠肠道动力，减轻结肠组织损伤，改善排便情况，其机制可能与激活SCF/c-Kit通路有关。

Objective To investigate the therapeutic effects and mechanisms of Aurantii Fructus Immaturus （AFI） on slow-transit constipation（STC） in mice. Methods A STC model was established via intragastric administration of Loperamide Hydrochloride. Successfully modeled mice were randomized into a model group，low-and high-dose AFI groups，a high-dose AFI + Masitinib[tyrosine kinase（c-Kit）inhibitor] group，additionally，a normal group was set up. After intervention， intestinal transit rate， 6-hour fecal pellet number， fecal water content， and colonic histomorphology（hematoxylin-eosin staining） were assessed. Enzyme-linked immunosorbent assay（ELISA） was used to measure levels of 5-hydroxytryptamine（5-HT），vasoactive intestinal polypeptide（VIP），substance P （SP），nitric oxide（NO），and nitric oxide synthase（NOS） activity in colon tissue. Quantitative real-time PCR （qRT-PCR） was used to evaluate mRNA expression of stem cell factor（SCF） and c-Kit in colon tissue，Western Blot was used to analyze relative protein expression of aquaporin 3（AQP3），aquaporin 8（AQP8），SCF，and c-Kit in colon tissue. Results Compared with the normal group，there was devere colonic damage observed in the colon tissue of the mice in the model group，the fecal pellet number，fecal water content，intestinal transit rate，colon tissue SP content，c-Kit and SCF gene and protein expression levels were reduced. The contents of 5-HT， VIP and NO，NOS activity and the protein expression levels of AQP3 and AQP8 in colon tissue were increased， and the differences were statistically significant（P＜0.05）. Compared with the model group，the colonic injury of mice in the low- and high- does AFI groups showed obvious improvement，the fecal pellet number，fecal water content，intestinal transit rate，colon tissue SP content，c-Kit and SCF gene and protein expression levels were increased， the contents of 5-HT， VIP and NO， NOS activity and the protein expression levels of AQP3 and AQP8 in colon tissue were decreased（P＜0.05）. Masitinib partially reversed the laxative effects of AFI （P＜0.05）. Conclusion AFI enhances intestinal motility，alleviates colonic injury，and improves defecation in STC mice， potentially via activation of the SCF/c-Kit pathway.

R285.5

国家中医药管理局第七批全国老中医药专家学术经验继承工作项目[国中医药人教函（2022）76号 ]；湖北省中医药管理局2023～ 2024年度中医药指导性项目（编号：ZY2023F001）；武汉市肛肠疾病中西医结合治疗临床医学研究中心项目（编号：武科[2023]123号）