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CNP signal pathway up-regulated in rectum of depressed rats and the interventional effect of Xiaoyaosan

机译:抑郁大鼠直肠CNP信号通路上调及逍遥散的干预作用

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AIM: To investigate the distribution and expression of C-type natriuretic peptide (CNP)atriuretic peptide receptor B (NPR-B) in the rectum of a rodent depression model and the interventional effect of Xiaoyaosan (XYS). METHODS: Male rats (n = 45) of clean grade (200 ± 20 g) were divided into five groups after one week of adaptive feeding: primary control, depression model, low dose XYS, middle dose XYS, and high dose XYS. The animal experiment continued for 3 wk. Primary controls were fed normally ad libitum. The rats of all other groups were raised in solitary and exposed to classic chronic mild unpredictable stimulation each day. XYS groups were perfused intragastrically with low dose, middle dose, and high dose XYS one hour before stimulation. Primary control and depression model groups were perfused intragastrically with normal saline under similar conditions as the XYS groups. Three weeks later, all rats were sacrificed, and the expression levels of CNP and NPR-B in rectum tissues were analyzed by immunohistochemistry, real-time polymerase chain reaction, and Western blotting. RESULTS: CNP and NPR-B were both expressed in the rectum tissues of all rats. However, the expression levels of CNP and NPR-B at both gene and protein levels in the depression model group were significantly higher when compared to the primary control group (n = 9; P n = 9; P CONCLUSION: The CNP/NPR-B pathway is upregulated in the rectum of depressed rats and may be one mechanism for depression-associated digestive disorders. XYS antagonizes this pathway at least partially.
机译:目的:探讨C型利钠肽(CNP)/利钠肽受体B(NPR-B)在啮齿类抑郁症模型直肠中的分布和表达以及逍遥散(XYS)的干预作用。方法:适应性喂养一周后,将清洁级(200±20 g)的雄性大鼠(n = 45)分为五组:主要对照,抑郁模型,低剂量XYS,中剂量XYS和高剂量XYS。动物实验持续了3周。正常对照组随意喂养。所有其他组的大鼠每天单独饲养,并接受经典的慢性轻度不可预测的刺激。刺激前一小时,以低剂量,中剂量和高剂量XYS灌胃XYS组。在与XYS组相似的条件下,向原发对照组和抑郁模型组灌胃生理盐水。 3周后,处死所有大鼠,并通过免疫组织化学,实时聚合酶链反应和蛋白质印迹分析直肠组织中CNP和NPR-B的表达水平。结果:CNP和NPR-B均在所有大鼠的直肠组织中表达。然而,与主要对照组相比,抑郁模型组在基因和蛋白质水平上的CNP和NPR-B表达水平显着更高(n = 9; P n = 9; P)。结论:CNP / NPR- B通路在抑郁大鼠的直肠中上调,可能是与抑郁相关的消化系统疾病的一种机制,XYS至少部分拮抗该通路。

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