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作 者:许惠娟[1] 刘慧慧[1] 滕超[1] 王艳杰[1] 王德山[1]
机构地区:[1]辽宁中医药大学,沈阳110847
出 处:《中国实验方剂学杂志》2012年第6期141-144,共4页Chinese Journal of Experimental Traditional Medical Formulae
基 金:国家重点基础研究发展计划(973计划)项目(2007CB512702)
摘 要:目的:探讨痛泻要方治疗腹泻型肠易激综合征(D-IBS)模型大鼠的作用机制。方法:健康雄性Wistar大鼠40只随机分为正常组、模型组、中药组、药抗组,采用应激与束缚的方法18 d复制肠易激综合征模型,造模成功后中药组和药抗组大鼠给予中药23.6 g.kg-1,ig 1次/d,连续7 d,药抗组第4天开始给予血管活性肠肽(VIP)受体拮抗剂35μg.kg-1,iv 1次/d,连续4 d。检测大鼠粪便含水量,采用RT-PCR法和SABC免疫组化法检测结肠组织水通道蛋白8(aquaporin 8,AQP8)的表达。结果:①大鼠粪便含水量:与正常组比较,模型组粪便含水量升高(P<0.01);与模型组比较,中药组粪便含水量降低(P<0.01);药抗组粪便含水量与模型组差异无统计学意义。②结肠组织AQP8:与正常组比较,模型组AQP8表达下调(P<0.01);与模型组比较,中药组AQP8表达上调(P<0.01);药抗组AQP8表达与模型组差异没有统计学意义。结论:痛泻要方治疗D-IBS的药理学机制可能通过VIP途径调节AQP8的表达实现。Objective: To study the mechanism of Tongxie Yaofang (TXYF) in rat model of diarrhea- predominant irritable bowel syndrome (D-IBS). Method: Forty male Wistar rats were divided randomly into normal group, model group, TXYF group, antagonism group. The rat D-IBS model was established by binding stress for 18 d, after D-IBS model was established suceesful, TXYF group and TXYF + antagonism group were orally given TXYF at a dose of 23.6 g· kg-1 , once a day for 7 d , meanwhile antagonism group was iv given vasoactine intrestinal peptide (VIP) antagomst at a dose of 35 g· kg-1 for once a day 4 d after 4 d of being given TXYF. The water content in rat feces was determined. The method of reverse transcription-polymerase chain reaction (RT-PCR) and immunohistochemistry was used to determine the expression of aquaporin-8 (AQP8) in colon tissue. Result: (!) The water content in rat feces, compared with normal group, in TXYF group was higer (P 〈0.01 ),and compared with model group, in TXYF group the water content was significantly reduced (P 〈0. 01), but in antagonism group no change was found. The colon model group, the expression of AQP8 in TXYF group was significantly group no change was observed. Conclusion: The mechanism of TXYF expression level of AQPS, compared with increased (P 〈 0.01 ), but in antagonism in treatment of D-IBS may be related toregulating the secretion of VIP and up-regulating the AQP8 expression in colon tissue.
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