论文部分内容阅读
目的:探讨穴位埋线治疗溃疡性结肠炎的作用机制.方法:将18只SD大鼠随机分为3组:正常对照组、模型组、穴位埋线组,每组6只.除正常对照组未行造模外,其余2组大鼠均采用三硝基苯磺酸(TNBS)造摸.模型组不予干预,正常饮食,穴位埋线组于“上巨虚”“天枢”“大肠俞”处进行穴位埋线治疗.治疗15 d后观察大鼠的腹泻、便血症状和结肠病理组织学改变,用western blot法检测大鼠脾淋巴细胞核因子-κB p65(NF-κB p65)及相关信号分子β2肾上腺素受体(β2AR)蛋白的表达.结果:穴位埋线组的大鼠腹泻、黏液脓血便症状得到较快控制,大鼠黏膜组织损伤明显改善;与正常对照组相比,模型组大鼠脾淋巴细胞NF-κB p65增多(P<0.01),β2AR的表达减少(P<0.01),两组差异有统计学意义;与模型组比较,穴位埋线组大鼠脾淋巴细胞NF-κB p65减少(P<0.01),而β2AR的表达增多(P<0.01),两组脾淋巴细胞NF-κB p65和β2AR的表达存在明显差异.结论:穴位埋线治疗实验性结肠炎有明显效果,其作用机制可能是通过调节NF-κB p65及相关信号分子β2AR,从而发挥治疗作用.“,”T Objective To investigate the mechanisms of catgut implantation at acupoints onulcerative colitis. Methods Eighteen SD rats were randomly divided into a normal control group (NC),a model group (MO) and a catgut implantation group (CI) with 6 rats in each group. Animals in groupMO and group CI were treated by trinitro-benzene-sulfonic acid (TNBS) to establish model with colitis.symptoms of diarrhea and bloody stool, and changes in histopathology were detected 15 days afterthe treatment. Expressions of splenic lymphocyte nuclear factor κB p65 (NF-κB p65) and correlatedsignaling molecules (β2AR) were detected by the western blot method. Results Diarrhea and mucusbloody purulent stool were soon controlled, and mucous injures were obviously improved in group CI.The NF-κB p65 value of splenic lymphocytes was significantly increased (P<0.01) and expression ofβ2AR remarkably reduced in group MO (P<0.01), compared with group NC. But, the NF-κB p65 valuewas significantly decreased (P<0.01) and expression of β2AR remarkably increased in group CI (P<0.01), compared with group MO. Conclusion Catgut implantation at acupoints is obviously effectivein treating experimental colitis. Modulation of NF-κB p65 and the correlated signaling molecules β2ARmay be involved in the mechanisms.