胃肠安丸通过调节脑-肠肽和肠道菌群减轻功能性消化不良。

Liao Mengting, L I Tao, Chu Fuhao, Chen Yan, Lou Ni, Zhuang Yuan, B O Rongqiang, Ding Xia
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摘要

目的:评价胃肠安丸(WCAP)对功能性消化不良(FD)的治疗作用,探讨其调节脑肠肽(BGPs)和肠道菌群平衡的可能机制。方法:除正常组外,采用“0℃生理盐水灌胃+不规则喂养夹尾”的方法建立FD大鼠模型。将成功建立的FD大鼠模型随机分为模型组和WCAP1 (WC1)、WCAP2 (WC2)、WCAP3 (WC3)、WCAP4 (WC4)、WCAP5 (WC5)、多潘立酮(Dom)组(每组10只)。未处理的大鼠作为对照组。采用炭推进法对大鼠胃肠运动进行评价。苏木精和伊红(HE)染色评价组织病理学。采用酶联免疫吸附法检测各组血清胃动素(MTL)、胃泌素(GAS)、血管活性肠肽(VIP)、生长抑素(SS)水平。此外,采用16S rRNA测序分析粪便样品的肠道微生物群组成。结果:根据大鼠状态、胃肠运动评估、HE染色等数据成功建立大鼠模型。WCAP通过促进FD大鼠胃排空和小肠运输改善FD症状。机制上,WCAP提高了GAS和MTL水平,降低了VIP和SS水平。此外,WCAP处理恢复了厚壁菌门和拟杆菌门的总相对丰度,增加了肠道菌群的物种丰富度,调节了肠道菌群组成和功能的变化。结论:WCAP能有效促进FD大鼠胃肠运动障碍的恢复。其机制可能与调节bgp的分泌和肠道菌群的组成有关。
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Weichang' an pill alleviates functional dyspepsia through modulating brain-gut peptides and gut microbiota.

Objective: To evaluate the effect of Weichang'an pill (, WCAP) on functional dyspepsia (FD) and explore its regulation of brain-gut peptides (BGPs) and gut microbiota balance as a potential treatment mechanism.

Methods: The "0 ℃ saline gavage + irregular feeding and tail clamp" method was used to establish the FD rat model, excluding the normal group. The successfully established FD rat models were randomly divided into the model group and the WCAP1 (WC1), WCAP2 (WC2), WCAP3 (WC3), WCAP4 (WC4), WCAP5 (WC5), and Domperidone (Dom) groups (n = 10 per group). The unhandled rats were designated as the control group. The gastrointestinal motility of the rats was evaluated using the charcoal propulsion test. Histopathology was assessed by hematoxylin and eosin (HE) staining. The enzyme-linked immunosorbnent assay method was used to detect the levels of motilin (MTL), gastrin (GAS), vasoactive intestinal peptide (VIP), and somatostatin (SS) in the serum from each group. In addition, the gut microbiota composition of fecal samples was analyzed using 16S rRNA sequencing.

Results: Rat models were successfully established according to data from rat state, gastrointestinal motility assessments, and HE staining. WCAP improved FD symptoms by accelerating the gastric emptying and small intestinal transit of FD rats. Mechanistically, WCAP increased the levels of GAS and MTL and reduced the levels of VIP and SS. Moreover, WCAP treatment restored the total relative abundance of Firmicutes and Bacteroidetes, increased the species richness of the gut flora, and modulated the changes in the composition and function of the gut microbiota.

Conclusion: WCAP can effectively promote the recovery of gastrointestinal motility disorders in FD rats. The mechanism may be related to regulating the secretion of BGPs and the composition of the gut microbiota.

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