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基于调节胃黏膜微生物群和炎症因子探讨胃转安对胃癌癌前病变大鼠的影响。

Effects of Weizhuan'an on rats with precancerous lesions of gastric cancer based on regulating gastric mucosal microflora and inflammatory factors.

作者信息

Lu Yuting, Liu Huayi, Shang Jiaju, Mao Yijia, Meng Lingkai, Gao Changbai

机构信息

Guangdong Second Provincial General Hospital, Integrated Chinese and Western Medicine Postdoctoral Research Station, School of Medicine, Jinan University, Guangzhou, Guangdong, China.

Graduate School, Tianjin University of Traditional Chinese Medicine, Tianjin, China.

出版信息

Front Pharmacol. 2024 Aug 16;15:1446244. doi: 10.3389/fphar.2024.1446244. eCollection 2024.

DOI:10.3389/fphar.2024.1446244
PMID:39221149
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11361960/
Abstract

OBJECTIVES

This study aimed to observe the intervention of Weizhuan'an prescription on rats with precancerous lesions of gastric cancer (PLGC) as well as its regulation on gastric mucosal microflora and inflammatory factors and explore the pharmacodynamic mechanisms of Weizhuan'an Formula.

METHODS

The rats were classified into the blank control group (BCG); low-, medium-, and high-dose groups of Weizhuan'an prescription (LDG, MDG, and HDG, respectively); and natural recovery group (NRG) at random. The rats in the traditional Chinese medicine (TCM) group were given corresponding doses of Weizhuan'an formula, while the rats in the NRG and BCG were given an equivalent volume of distilled water for 12 weeks. After that, gastric mucosa samples of rats were collected to observe the general and pathological changes in the gastric mucosa; the changes in gastric mucosal microflora were detected by 16S rDNA amplicon sequencing, and the inflammatory factors were analyzed by cytokine antibody microarray and Western blotting.

RESULTS

The results suggest that compared with the BCG, the pathology of gastric mucosa and gastric mucosal microflora and inflammatory factors in rats with PLGC have changed significantly, while Weizhuan'an formula effectively improved them, especially in the MDG and HDG ( < 0.05). Compared with the NRG, the abundance of probiotics such as and were increased, while the abundance of pathogens such as and was decreased ( < 0.05, < 0.01), and the relative contents of IL-2, IL-4, IL-13, and MCP-1 in gastric mucosa were decreased ( < 0.05). Moreover, it can upregulate the DNA-binding transcriptional regulator, ABC type multidrug transport system, and related enzymes and affect the signaling pathways such as viral protein interaction with cytokine and cytokine receptor and T cell receptor signaling pathway significantly ( < 0.05, < 0.01), which can promote drug absorption and utilization and repair damaged gastric mucosa.

CONCLUSION

The study confirmed that Weizhuan'an prescription can treat rats with PLGC by regulating gastric mucosal microflora and inflammatory factors.

摘要

目的

本研究旨在观察胃转安方对胃癌前病变(PLGC)大鼠的干预作用及其对胃黏膜微生物群和炎症因子的调节作用,探讨胃转安方的药效机制。

方法

将大鼠随机分为空白对照组(BCG)、胃转安方低、中、高剂量组(分别为LDG、MDG和HDG)和自然恢复组(NRG)。中药组大鼠给予相应剂量的胃转安方,NRG组和BCG组大鼠给予等体积蒸馏水,持续12周。之后,采集大鼠胃黏膜样本,观察胃黏膜的大体和病理变化;采用16S rDNA扩增子测序检测胃黏膜微生物群的变化,通过细胞因子抗体芯片和蛋白质免疫印迹法分析炎症因子。

结果

结果表明,与BCG组相比,PLGC大鼠的胃黏膜病理、胃黏膜微生物群和炎症因子均发生了显著变化,而胃转安方有效改善了这些变化,尤其是MDG组和HDG组(P<0.05)。与NRG组相比,双歧杆菌属和乳杆菌属等益生菌的丰度增加,而肠杆菌属和拟杆菌属等病原菌的丰度降低(P<0.05,P<0.01),胃黏膜中IL-2、IL-4、IL-13和MCP-1的相对含量降低(P<0.05)。此外,它可上调DNA结合转录调节因子、ABC型多药转运系统及相关酶,并显著影响病毒蛋白与细胞因子和细胞因子受体相互作用以及T细胞受体信号通路等信号通路(P<0.05,P<0.01),从而促进药物吸收利用,修复受损胃黏膜。

结论

本研究证实胃转安方可通过调节胃黏膜微生物群和炎症因子治疗PLGC大鼠。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/797b/11361960/ecc67b4b737d/fphar-15-1446244-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/797b/11361960/ff4312efb09c/fphar-15-1446244-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/797b/11361960/89b56f4adee5/fphar-15-1446244-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/797b/11361960/01ac57ae40f2/fphar-15-1446244-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/797b/11361960/25a074e4ec2e/fphar-15-1446244-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/797b/11361960/ecc67b4b737d/fphar-15-1446244-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/797b/11361960/ff4312efb09c/fphar-15-1446244-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/797b/11361960/89b56f4adee5/fphar-15-1446244-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/797b/11361960/01ac57ae40f2/fphar-15-1446244-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/797b/11361960/25a074e4ec2e/fphar-15-1446244-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/797b/11361960/ecc67b4b737d/fphar-15-1446244-g005.jpg

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