Effect of Si Junzitang on CaM-MLCK Pathway in Rats with Spleen Deficiency and Gastrointestinal Motility Disorder

ZHONG Zi-shao; ZHANG Hai-yan; ZHANG Wang; HE Gui-hua; YE Zhen-hao; Wang Jing; HUANG Sui-ping

doi:10.13422/j.cnki.syfjx.2018050095

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Effect of Si Junzitang on CaM-MLCK Pathway in Rats with Spleen Deficiency and Gastrointestinal Motility Disorder

更新时间：2024-01-04

- Effect of Si Junzitang on CaM-MLCK Pathway in Rats with Spleen Deficiency and Gastrointestinal Motility Disorder
- Chinese Journal of Experimental Traditional Medical Formulae Vol. 24, Issue 5, Pages: 95-99(2018)
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- DOI：10.13422/j.cnki.syfjx.2018050095
  CLC： R285.5
- Published：2018
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ZHONG Zi-shao, ZHANG Hai-yan, ZHANG Wang, et al. Effect of Si Junzitang on CaM-MLCK Pathway in Rats with Spleen Deficiency and Gastrointestinal Motility Disorder[J]. Chinese journal of experimental traditional medical formulae, 2018, 24(5): 95-99.
DOI：

ZHONG Zi-shao, ZHANG Hai-yan, ZHANG Wang, et al. Effect of Si Junzitang on CaM-MLCK Pathway in Rats with Spleen Deficiency and Gastrointestinal Motility Disorder[J]. Chinese journal of experimental traditional medical formulae, 2018, 24(5): 95-99. DOI： 10.13422/j.cnki.syfjx.2018050095.

摘要

目的：通过实验探讨脾虚证胃肠动力障碍（gastrointestinal dysfunction，GID）的发病及四君子汤干预的作用机制。方法：将36只SD大鼠随机分为空白组、模型组、中药组和西药组，运用碘乙酰胺灌服+小平台站立+饥饱失常法塑造脾虚证GID动物模型，随后给予中药组四君子汤6.3 g · kg-1和西药莫沙必利0.45 mg · kg-1灌胃，通过胃排空测定、蛋白免疫印迹法（Western blot），免疫组化法，实时荧光定量PCR法（Real-time PCR）及Mg2+-ATPase活性检测对各组大鼠胃排空率及钙调素（CaM）-肌球蛋白轻链激酶（MLCK）通路改变进行检测。结果：模型组大鼠胃排空率较正常大鼠低（P<0.01），平滑肌CaM，MLCK蛋白表达量，MLCK mRNA及MLCK活性升高（P<0.05，P<0.01）；四君子汤干预后大鼠胃排空率升高（P<0.05），平滑肌CaM，MLCK蛋白，MLCK mRNA表达量及MLCK活性升高（P<0.05，P<0.01）。结论：脾虚证GID大鼠存在CaM-MLCK信号通路改变，四君子汤可能通过调节该信号通路舒缓胃平滑肌高张力而间接促进胃肠动力。

Abstract

Objective:To investigate the pathogenesis of gastrointestinal dysfunction (GID) with spleen deficiency syndrome and the intervention effect of Si Junzitang. Method:Totally 36 rats were randomly divided into control group

model group

Si Junzitang group and mosapride group. Iodoacetamide gavage+small platform standing+irregular feeding were used to establish the rat model with spleen deficiency and gastrointestinal dysfunction. After modeling

Si Junzitang (6.3 g·kg-1) and mosapride (0.45 mg·kg-1) were given to intervention groups by gavage; subsequently

gastric emptying detection

Western blot

immunohistochemical staining

Real-time PCR and Mg2+-ATPase activity detection were performed to detect the changes in Calmodulin (CaM)-myosin light chain kinase (MLCK) pathway. Result:Compared with normal group

weight and gastric emptying rate were lower (P<0.01)

and CaM and MLCK protein and mRNA expressions and Mg2+-ATPase activity of gastric antral smooth muscle were higher in model group (P<0.05

P<0.01). Compared with model group

weight and gastric emptying rate were higher (P<0.05)

and CaM and MLCK protein and mRNA expressions and Mg2+-ATPase activity were lower in Si Junzitang group and mosapride group (P<0.05

P<0.01). Conclusion:Rats with spleen deficiency and gastrointestinal dysfunction show CaM-MLCK pathway disorder. Si Junzitang may indirectly improve gastric motility by regulating CaM-MLCK pathway.

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