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Effects of vibrating the abdomen on peripheral blood gastrointestinal hormones and gastrointestinal motility of young anorexia model rats

振腹对幼龄厌食模型大鼠外周血中胃肠激素及胃肠动力的影响

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Abstract

Objective

To observe the therapeutic effect of vibrating the abdomen on anorexia model rats, as well as its effects on cholecystokinin octapeptide (CCK-8) and motilin (MTL) in the peripheral blood.

Methods

Forty young rats were randomly divided into a normal group (n=10) and a modeling group (n=30). Rats in the normal group were fed common feed. The anorexia model was established by the etiological simulation method in the modeling group, and these rats were further randomly divided into a drug group, a vibrating abdomen group, and a model group 3 weeks after the anorexia model was induced, with 10 rats in each group. The drug group was given Jian Wei **ao Shi Pian by intragastric administration at a dose of 0.72 g/(kg·bw) (0.72 g drug was dissolved in 10 mL purified water). The normal group and the model group were given purified water once a day in the morning. The vibrating abdomen group was treated with vibrating the abdomen once a day for 21 times. The body mass, food intake, serum CCK-8, MTL, gastrin (GAS), neurotensin (NT) levels, and the intestinal propulsion rate of rats in each group were measured.

Results

Compared with the model group, the body mass, food intake, serum MTL and GAS levels, and the small intestine propulsion rate were significantly increased, and the serum CCK-8 and NT levels, the gastric residual rate decreased significantly in the vibrating abdomen group and the drug group (P<0.05). There was no significant difference between the vibrating abdomen group and the drug group (P>0.05).

Conclusion

Vibrating the abdomen increases the food intake and body mass of anorexia model rats, reduces the residue of gastric contents, improves the small intestine propulsion rate, and therefore has a good therapeutic effect on anorexia. The mechanism may be related to inhibiting the secretion of CCK-8 and NT in plasma and promoting the release of MTL and GAS in serum.

摘要

目的

观察振腹对厌食症模型大鼠的治疗作用及对其外周血中八肽胆囊收缩素(CCK-8)和胃动素(MTL)含量的影响。

方法

按照随机数字表法将40只幼龄大鼠进行分组, 分为**常组10只和造模组30只。**常组给予普通饲料喂食。造模组采用病因模拟法构建厌食症模型, 造模3周后将其随机分为药物组、振腹组和模型组, 每组10只。药物组按0.72 g/(kg·bw)剂量给予健胃消食片灌胃(将0.72 g药物用纯水配制成10 mL药液); **常组和模型组等体积每天上午灌服纯水1次; 振腹组予以振腹治疗, 每日1次, 共治疗21次。检测各组大鼠体质量、摄食量、外周血CCK-8、MTL、胃泌素(GAS)及神经降压素(NT)的含量和小肠推进率。

结果

与模型组相比, 振腹组与药物组的体质量和摄食量、血清MTL及GAS含量和小肠推进率明显提高, 血浆CCK-8、NT含量及胃残留率降低, 差异具有统计学意义(P<0.05);但振腹组与药物组比较无统计学差异(P>0.05)。

结论

振腹可增加厌食症模型大鼠的进食量和体质量, 减少胃内容物的残留,提高小肠推进率, 对厌食症具有较好的治疗作用。其作用机理可能与抑制血浆CCK-8和NT分泌, 促进血清MTL和GAS释放有关。

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Acknowledgments

This work was supported by the Project of Hebei Provincial Administration of Traditional Chinese Medicine (河北省中医药管理局项目, No. 2017002).

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Authors and Affiliations

  1. Hebei University of Chinese Medicine, Shijiazhuang, 050200, China

    Ling Zhou  (周玲), Yan Zhang  (张岩), Liyun Yang  (杨丽芸) & **long Li  (**进龙)

  2. Hebei Province Special Care Hospital, Shijiazhuang, 050051, China

    Nan Gu  (谷楠)

  3. The Third Hospital of Shijiazhuang, Hebei Province, Shijiazhuang, 050011, China

    Weijie Bai  (白卫杰)

Authors
  1. Ling Zhou  (周玲)
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  2. Yan Zhang  (张岩)
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  3. Nan Gu  (谷楠)
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  4. Weijie Bai  (白卫杰)
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  5. Liyun Yang  (杨丽芸)
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  6. **long Li  (**进龙)
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Corresponding author

Correspondence to **long Li  (**进龙).

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The authors declare that there is no potential conflict of interest in this article.

Statement of Human and Animal Rights

This study has been approved by the Ethics Committee of Hebei University of Chinese Medicine (Approval No. DWLL2020115). The treatment of animals in this experiment conformed to the ethical criteria. V)

Additional information

Co-first Authors: ZHOU Ling, master degree candidate of 2020; ZHANG Yan, lecturer

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Zhou, L., Zhang, Y., Gu, N. et al. Effects of vibrating the abdomen on peripheral blood gastrointestinal hormones and gastrointestinal motility of young anorexia model rats. J. Acupunct. Tuina. Sci. 22, 104–110 (2024). https://doi.org/10.1007/s11726-023-1413-1

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  • DOI: https://doi.org/10.1007/s11726-023-1413-1

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