痛泻要方对肝郁脾虚型腹泻型肠易激综合征大鼠肠道高敏性的治疗作用

Therapeutic Effects of Tongxie Yaofang Decoction on Intestinal Hypersensitivity of Diarrhea Predominant Irritable Bowel Syndrome Rats with Liver-stagnation and Spleen-deficiency Pattern

关键词:  痛泻要方  腹泻型  肠易激综合征  肠道高敏性  下丘脑-垂体-肾上腺轴(HPA轴)  p38丝裂原活化蛋白酶磷酸化  cAMP反应原件结合蛋白

Key words:  Tongxie Yaofang decoction  diarrhea-predominan  irritable bowel syndrome  intestinal hypersensitivity  HPA axis  p-p38 MAPK  CREB

摘要:

目的 研究痛泻要方对肝郁脾虚型腹泻型肠易激综合征(diarrhea predominant irritable bowel syndrome,D-IBS)大鼠肠道高敏性的治疗作用。方法 采用番泻叶灌服与慢性束缚建立肝郁脾虚型D-IBS大鼠模型,观察痛泻要方对肝郁脾虚型D-IBS大鼠HPA轴的相关指标促肾上腺皮质激素释放激素(corticotropin releasing hormone,CRH)、血浆促肾上腺皮质激素(adrenocorticotropic hormone,ACTH)、皮质醇(cortisol,CORT),结肠组织中p38 MAPK、MSK1磷酸化及cAMP反应原件结合蛋白(cyclic-AMP response binding protein,CREB)表达水平的影响。结果 痛泻要方可以降低肝郁脾虚型D-IBS大鼠CRH、ACTH、CORT含量,抑制结肠组织中p38MAPK,MSK1磷酸化及CREB蛋白的表达,尤以痛泻要方高剂量组最为显著(P<0.05或P<0.01)。结论 痛泻要方对番泻叶灌服与慢性束缚建立的肝郁脾虚型D-IBS大鼠肠道敏感性具有显著降低的作用,其机制可能与下调p38 MAPK、MSK1磷酸化和CREB蛋白的表达,抑制HPA轴亢进有关。

Abstract:

OBJECTIVE To investigate the effect of Tongxie Yaofang decoction on intestinal hypersensitivity in diarrhea predominant irritable bowel syndrome(D-IBS) rats with liver-stagnation and spleen-deficiency pattern.METHODS D-IBS rat model of liver depression and spleen deficiency was established by perfusing Senna Folium and chronic restraint, then to observe the effects of Tongxie Yaofang decoction on the related indexes of HPA axis corticotropin releasing hormone(CRH), adrenocorticotropic hormone(ACTH), cortisol(CORT), p38 MAPK, MSK1 phosphate and cyclic-AMP response binding protein(CREB) expression in colon tissues.RESULTS Tongxie Yaofang decoction could reduce the contents of CRH, ACTH, CORT, and inhibit p38 MAPK, MSK1 phosphorylation and CREB protein expression in colon tissue of D-IBS rats with liver depression and spleen deficiency type, especially in the high dose group of Tongxie Yaofang decoction(P<0.05 or P<0.01).CONCLUSION Tongxie Yaofang decoction can anti-abdominal pain effect on D-IBS rats of chronic restraint and liver stagnation and spleen deficiency type after oral administration of Senna Folium. The mechanism is related to down-regulation of p38 MAPK, MSK1 phosphorylation and CREB protein expression, and inhibition of HPA axis hyperfunction.