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作 者:刘丽娟[1,2] 王允亮[1] 魏仕兵[1] 杨美娟[3] 李军祥[1]
机构地区:[1]北京中医药大学东方医院,北京100078 [2]中日友好医院,北京100029 [3]北京中医药大学,北京100029
出 处:《中华中医药杂志》2015年第9期3266-3269,共4页China Journal of Traditional Chinese Medicine and Pharmacy
基 金:北京中医药大学创新团队资助项目(No.2011-CXTD-24);北京中医药大学大学生自主课题(No.2014-JYBZZ-XS-152)~~
摘 要:目的:研究清肠温中方对2,4,6-三硝基苯磺酸(TNBS)诱导的溃疡性结肠炎大鼠的疗效及作用机制。方法:以TNBS/乙醇灌肠诱导大鼠溃疡性结肠炎,造模成功后连续以清肠温中方(QCWZD)高、中、低剂量及柳氮磺吡啶(SASP)混悬液灌胃干预10d,取结肠,评价疾病活动指数(DAI),酶联免疫吸附法检测血清白介素-6(IL-6)、肿瘤坏死因子-α(TNF-α)水平,免疫组织化学法检测occludin蛋白、带状闭合蛋白-1(ZO-1)在结肠黏膜的分布及表达。结果:模型组DAI评分、血清IL-6、TNF-α水平明显高于正常组(P<0.05),肠黏膜occludin、ZO-1表达总量低于正常组(P<0.01);清肠温中方各剂量组DAI水平较模型组明显下降(P<0.05);清肠温中方低剂量组血清IL-6水平均较模型组明显下降(P<0.05),清肠温中方高、中剂量组血清TNF-α水平均较模型组明显下降(P<0.05);清肠温中方高、中剂量组肠黏膜occludin、ZO-1蛋白表达总量显著高于模型组(P<0.01)。结论:清肠温中方能通过下调血清IL-6、TNF-α水平,升高肠黏膜occludin、ZO-1蛋白总量的表达,起到修复TNBS诱导的溃疡性结肠炎大鼠肠黏膜损伤的作用。Objective: To investigate the mechanism of Qingchang Wenzhong Decoction (QCWZD) in colitis rats induced by 2,4,6-trinitrobenzene sulfonic acid (TNBS). Methods: Experimental colitis was induced in male sprague-dawley (SD) rats by intracolonic administration of TNBS/alcohol. High, medium, and low doses of QCWZD and salazosulfapyridine (SASP) was given by gavage route daily for 10 days. Disease activity index (DAI) was estimated. Serum IL-6 and TNF-α level was detected by Elisa assay. Occludin and ZO-1 in colonic mucosa were detected by immunological histological chemistry assay. Results: DAI and serum IL-6, TNF-α level were significantly higher in TNBS-treated rats than normal group (P〈0.05), while expression of occluding and ZO-1 was significantly reduced (P〈0.01). DAd in QCWZD groups (1 200mg/kg, 600mg/kg, 300mg/kg) decreased significantly compared with model group (P〈0.05). Serum IL-6 expression was reduced in low dose QCWZD (300mg/Kg) group (P〈0.05), and TNF-α expression was reduced in high and medium dose QCWZD (1200mg/kg, 600mg/kg) groups. Expression of occludin and ZO-1 in colonic mucosa was significantly increased in QCWZD (1200mg/kg, 600mg/kg) groups than model group (P〈0.01). Conclusion: QCWZD could repair colonic mucosal damage of TNBS-induced colitis rats by down-regulating serum IL-6, TNF-α expression and increasing occludin and ZO-1 expression in colonic mucosa.
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