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目的:探讨脾虚证功能性消化不良的发病及四君子汤干预的作用机制。方法:将52只SD大鼠随机分为空白组、模型组、四君子汤组和莫沙必利组,采用碘乙酰胺灌服+小平台站立+饥饱失常法塑造脾虚证功能性消化不良动物模型,随后给予四君子汤6.3 g·kg~(-1)和莫沙必利0.45 mg·kg-1灌胃,每日灌胃给药1次,共14 d,检测大鼠胃排空率,采用酶联免疫吸附测定法(ELISA)检测血清C型钠尿肽(CNP)及胃窦平滑肌组织环磷酸鸟苷(cGMP)含量,蛋白质免疫印迹法(Western blot)检测胃平滑肌B型钠尿肽受体(NPRB)蛋白的表达。结果:与正常组比较,模型组大鼠体重、胃排空率明显下降(P<0.05,P<0.01),血清CNP含量,平滑肌NPRB蛋白的表达和c GMP含量升高(P<0.05,P<0.01);与模型组比较,四君子汤和莫沙必利干预后大鼠胃排空率升高(P<0.05),血清CNP含量、平滑肌NPRB蛋白的表达量和c GMP含量降低(P<0.05,P<0.01)。结论:脾虚证功能性消化不良大鼠存在CNP-NPRB-c GMP信号通路改变,四君子汤可能通过调节该信号通路促进胃肠动力。
Objective: To explore the pathogenesis of functional dyspepsia in spleen deficiency syndrome and the mechanism of Sijunzi Decoction intervention. Methods: Fifty-two SD rats were randomly divided into blank group, model group, Sijunzi Decoction group and mosapride group. The iodine-acetamide perfusion plus small platform standing + Model, and then given Sijunzi Decoction 6.3 g · kg ~ (-1) and mosapride 0.45 mg · kg-1 orally, once daily gavage for 14 days to detect gastric emptying rate, Serum C-type natriuretic peptide (CNP) and cGMP in gastric smooth muscle were detected by enzyme-linked immunosorbent assay (ELISA). The levels of cGMP in gastric smooth muscle were detected by Western blot. Receptor (NPRB) protein expression. Results: Compared with the normal group, the body weight and the gastric emptying rate of the model group were significantly decreased (P <0.05, P <0.01), the CNP content, the expression of NPRB protein and the content of c GMP increased <0.01). Compared with the model group, the gastric emptying rate of rats after Sijunzi Decoction and mosapride intervention were increased (P <0.05), the content of CNP, the expression of NPRB protein and the content of c GMP decreased (P < 0.05, P <0.01). CONCLUSION: There is CNP-NPRB-c GMP signaling pathway in functional dyspepsia rats with spleen deficiency syndrome. Sijunzi Decoction may promote gastrointestinal motility by regulating this signaling pathway.