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纸质出版日期:2012
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许惠娟, 刘慧慧, 滕超, 等. 痛泻要方对腹泻型肠易激综合征模型大鼠结肠水通道蛋白8表达影响的机制研究[J]. 中国实验方剂学杂志, 2012,18(6):141-144.
XU Hui-juan, LIU Hui-hui, TENG Chao, et al. Regulation of Tongxie Yaofang on Aquaporin-8 in Colon Tissue of Rats with Irritable Bowel Syndrome[J]. Chinese journal of experimental traditional medical formulae, 2012, 18(6): 141-144.
许惠娟, 刘慧慧, 滕超, 等. 痛泻要方对腹泻型肠易激综合征模型大鼠结肠水通道蛋白8表达影响的机制研究[J]. 中国实验方剂学杂志, 2012,18(6):141-144. DOI:
XU Hui-juan, LIU Hui-hui, TENG Chao, et al. Regulation of Tongxie Yaofang on Aquaporin-8 in Colon Tissue of Rats with Irritable Bowel Syndrome[J]. Chinese journal of experimental traditional medical formulae, 2012, 18(6): 141-144. DOI:
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35 μg·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) antagonist at a dose of 35 μg·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: ① 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. ②The colon expression level of AQP8
compared with model group
the expression of AQP8 in TXYF group was significantly increased (P<0.01)
but in antagonism group no change was observed. Conclusion: The mechanism of TXYF in treatment of D-IBS may be related to regulating the secretion of VIP and up-regulating the AQP8 expression in colon tissue.
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