肠康颗粒对腹泻型肠易激综合征大鼠的药效学研究

目的 观察肠康颗粒对腹泻型肠易激综合征(IBS-D)模型大鼠的治疗作用，初步探讨其作用机制。方法 乳大鼠出生后第8~21天，每天接受直结肠扩张刺激建立IBS-D内脏高敏感模型。60只大鼠随机分为6组，即正常对照组、模型对照组、阳性药组、肠康颗粒高、中、低剂量组，连续30d分别灌胃给药。进行腹壁撤退反射(AWR)评分。酶联免疫分析法检测大鼠血清降钙素基因相关肽（CGRP），大鼠结肠组织血管活性肠肽（VIP）。免疫组化法测定大鼠结肠黏膜层血管P物质（SP）阳性表达。结果 与正常对照组比较，模型对照组大鼠AWR评分明显升高（P<0.01），血清CGRP含量、结肠组织VIP含量及结肠黏膜层血管SP阳性表达细胞数均显著降低（P<0.01）。与模型对照组比较，肠康颗粒各组大鼠的AWR评分明显降低（P<0.01），血清CGRP含量、结肠组织VIP含量明显升高（P<0.05～0.01），肠康颗粒中、高剂量组大鼠结肠黏膜层血管SP阳性表达细胞数明显的升高（P<0.05～0.01）。结论 肠康颗粒对IBS-D大鼠有一定治疗作用。其作用机制可能与抑制IBS-D大鼠血清CGRP及结肠组织VIP含量的下降，抑制大鼠结肠黏膜层血管SP阳性表达下降有关。 

Pharmacodynamics of Changkang Granules in IBS-D Rats

OBJECTIVE To study the therapeutic effect of Changkang Granules in rat with irritable bowel syndrome with Diarrhea （IBS-D) and investigate its mechanism． METHODS The model for IBS-D was established by colorectal distention daily in the neonatal rats between postnatal 8 and 21 days. Sixty SD rats were divided into the normal control group，the model group，positive control group，high-dose，middle-dose，low-dose Changkang Granules group．The treatment lasted for 30 days． The threshold of abdominal withdrawal reflex(AWR) during rectal distension was evaluated. The calcitonin gene-related peptide（CGRP） in serum， vasoactive intestinal peptide（VIP） in colon homogenates were evaluated by radioimmunoassay．Immunohistochemical SABC method to observe expression level of SP of colonic specimens. RESULTS Compared with the normal control group，AWR score increased（P<0.01）， The content of serum CGRP， VIP levels in colonic homogenate and expression level of SP in colon decreased markedly in the model group（P<0.01）. After administration with Changkang Granules， the AWR scores of the IBS-D rats were reduced（P<0.01）. The content of serum CGRP， colon VIP level and expression of SP in colon was increased significantly（P<0.05～0.01）. CONCLUSION The therapeutic effect of Changkang Granules on IBS-D rat is obvious． The mechanism could be related to inhibition against the excessive decrease of serum CGRP， colon VIP and expression level of SP in colon in IBS-D rats．