Background/Aims:This study was designed to investigate the effect of Fengliao-Changweikang (FLCWK) in diarrhea-predominant irritable bowel syndrome (IBS-D) rats and explore its underlying mechanisms.
Methods:IBS-D model rats were induced by neonatal maternal separation (NMS) combined with restraint stress (RS). In in vivo experiments, the model rats were randomly divided into 5 groups: NMS + RS, FLCWK (low dose, middle dose, and high dose), and pinaverium bromide. The normal control (no handling) rats were classified as the NH group. The therapeutic effect of FLCWK was evaluated by fecal characteristics, electromyographic response and abdominal withdrawal reflex scores. In in vitro experiments, the model rats were randomly divided into 2 groups: NMS + RS, FLCWK (middle dose), and no handling rats were used as the NH group. The differences in basic tension and ACh-induced tension of isolated colonic longitudinal smooth muscle strips (CLSMs) among the 3 groups were observed. In addition, different inhibitors (nifedipine, TMB-8, L-NAME, methylene blue, and 4-AP) were pretreated to explore the underlying mechanisms.
Results:In in vivo experiments, fecal characteristics, electromyographic response, and abdominal withdrawal reflex scores significantly improved in the FLCWK group, compared with the NMS + RS group. In in vitro experiments, the basic tension and ACh-induced tension of CLSMs in IBS-D rats were significantly inhibited by FLCWK. After pre-treatment with different inhibitors, the ACh-induced tension of CLSMs in each group showed no significant difference.
Conclusions:FLCWK manifested curative effect in IBS-D rats by inhibiting colonic contraction. The underlying mechanisms may be related to regulatory pathway of nitric oxide/cGMP/Ca²⁺ and specific potassium channels.
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【Effects of Fengliao-Changweikang in Diarrhea-predominant Irritable Bowel Syndrome Rats and Its Mechanism Involving Colonic Motility.].
【丰辽常味康对腹泻型肠易激综合征大鼠的作用及其与结肠运动的关系。】
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DOI：10.5056/jnm17093文章类型：杂志文章
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背景/目的：本研究旨在研究风腹常微康（FLCWK）对腹泻型肠易激综合征（IBS-D）大鼠的作用，并探讨其潜在机制。
方法：采用母体分离（NMS）联合束缚应激（RS）诱导IBS-D模型大鼠。在体内实验中，将模型大鼠随机分为5组：NMS RS，FLCWK（低剂量，中剂量和高剂量）和吡那溴铵。正常对照（不处理）大鼠被分类为NH组。通过粪便特征，肌电图反应和腹部缩回反射评分评估FLCWK的治疗效果。在体外实验中，将模型大鼠随机分为2组：NMS RS，FLCWK（中剂量），不使用任何处理的大鼠作为NH组。观察到3组之间的基本张力和ACh诱导的孤立结肠纵向平滑肌条（CLSM）张力的差异。此外，还对不同的抑制剂（硝苯地平，TMB-8，L-NAME，亚甲基蓝和4-AP）进行了预处理，以探索其潜在机理。
结果：在体内实验中，与NMS RS组相比，FLCWK组的粪便特性，肌电图反应和腹部退缩反射评分显着改善。在体外实验中，FLCWK显着抑制了IBS-D大鼠CLSMs的基本张力和ACh诱导的张力。在用不同的抑制剂进行预处理后，每组中由ACh诱导的CLSM的张力均无显着差异。
结论：FLCWK通过抑制结肠收缩对IBS-D大鼠具有治疗作用。潜在的机制可能与一氧化氮/ cGMP / Ca 2+和特定钾通道的调节途径有关。
方法：采用母体分离（NMS）联合束缚应激（RS）诱导IBS-D模型大鼠。在体内实验中，将模型大鼠随机分为5组：NMS RS，FLCWK（低剂量，中剂量和高剂量）和吡那溴铵。正常对照（不处理）大鼠被分类为NH组。通过粪便特征，肌电图反应和腹部缩回反射评分评估FLCWK的治疗效果。在体外实验中，将模型大鼠随机分为2组：NMS RS，FLCWK（中剂量），不使用任何处理的大鼠作为NH组。观察到3组之间的基本张力和ACh诱导的孤立结肠纵向平滑肌条（CLSM）张力的差异。此外，还对不同的抑制剂（硝苯地平，TMB-8，L-NAME，亚甲基蓝和4-AP）进行了预处理，以探索其潜在机理。
结果：在体内实验中，与NMS RS组相比，FLCWK组的粪便特性，肌电图反应和腹部退缩反射评分显着改善。在体外实验中，FLCWK显着抑制了IBS-D大鼠CLSMs的基本张力和ACh诱导的张力。在用不同的抑制剂进行预处理后，每组中由ACh诱导的CLSM的张力均无显着差异。
结论：FLCWK通过抑制结肠收缩对IBS-D大鼠具有治疗作用。潜在的机制可能与一氧化氮/ cGMP / Ca 2+和特定钾通道的调节途径有关。
