Jian-Pi-Yi-Shen formula improves kidney function by regulating gut microbiome in rats with chronic kidney disease.

IF 4.8 2区医学 Q2 IMMUNOLOGY

Frontiers in Cellular and Infection Microbiology Pub Date : 2025-07-09 eCollection Date: 2025-01-01 DOI:10.3389/fcimb.2025.1526863

Yuzhi Wang, Jiandong Lu, Wenkui Dai, Shudong Yang

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引用次数: 0

Abstract

Introduction: Recent studies have underscored the role of interactions between Traditional Chinese Medicine (TCM) and the gut microbiome (GM) in mediating therapeutic effects. Jian-Pi-Yi-Shen Formula (JPYSF) has shown efficacy in ameliorating chronic kidney disease (CKD) symptoms, but its mechanisms via GM modulation remain unclear.

Methods: In this study, 8-week-old rats were assigned to three groups after a two-week acclimation: C (normal diet for six weeks), M (adenine diet for four weeks then normal diet for two weeks), and T (same as M, with JPYSF administered during the final three weeks). Fecal samples were collected at three timepoints (T1: post-acclimation; T2: after three weeks on respective diets; T3: after three weeks of JPYSF treatment) for metagenomic sequencing. Serum creatinine (SCR) was measured at T2 and T3.

Results: At T2, adenine-fed rats showed elevated SCR (C: 28.4 ± 1.5 µmol/L; M: 189.6 ± 25.8µmol/L; T: 186.4 ± 32.5µmol/L; p < 0.001). By T3, SCR decreased more in T (86.0 ± 14.9µmol/L) than in M (119.6 ± 16.3µmol/L; p = 0.012), with C remaining stable (30.8 ± 4.4µmol/L). Adenine feeding induced significant GM shifts, evidenced by increased Aitchison distance (p < 0.01) and altered co-abundance interaction groups (CIGs): CIG3, 6, 9, 10 increased; CIG1, 2, 4, 12 decreased (all p < 0.05). After JPYSF treatment, only CIG4 significantly rebounded (T3 vs. M, p = 0.0079), and T3-T1 dissimilarity was lower in T than M (p < 0.05). SCR levels were significantly lower in T than M after returning to a normal diet, suggesting a renoprotective effect of JPYSF. Co-occurrence analysis linked SCR positively with toxin-associated CIGs (CIG3, 6, 7, 9, 10) and pathways (purine metabolism, toluene degradation), and negatively with CIG4.

Discussion: These results demonstrate that JPYSF lowers SCR and selectively modulates GM modules, particularly CIG4, which inversely correlates with uremic toxin-producing pathways, suggesting improved renal function and specific gut microbiota modulation in CKD rats.

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健脾益肾方通过调节慢性肾病大鼠肠道微生物群改善肾功能。

近年来的研究强调了中药（TCM）和肠道微生物组（GM）之间的相互作用在介导治疗效果中的作用。健脾益肾方（JPYSF）已显示出改善慢性肾脏疾病（CKD）症状的疗效，但其通过转基因调节的机制尚不清楚。方法：8周龄大鼠经过2周的驯化后，分为3组：C组（正常饮食6周），M组（腺嘌呤饮食4周，再正常饮食2周），T组（与M组相同，最后3周给予JPYSF）。在三个时间点采集粪便样本(T1：驯化后；T2：在各自饮食三周后；T3: JPYSF治疗三周后)进行宏基因组测序。在T2和T3时测定血清肌酐（SCR）。结果：在T2时，腺嘌呤喂养大鼠SCR升高(C: 28.4 ± 1.5 µmol/L；25.8µM: 189.6 ± mol / L;T: 186.4 ±32.5µ mol / L;p 讨论：这些结果表明JPYSF降低SCR并选择性调节GM模块，特别是与尿毒症毒素产生途径负相关的CIG4，这表明CKD大鼠的肾功能和特异性肠道微生物群调节得到改善。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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来源期刊

Frontiers in Cellular and Infection Microbiology IMMUNOLOGY-MICROBIOLOGY

CiteScore

7.90

自引率

7.00%

发文量

1817

审稿时长

14 weeks

期刊介绍： Frontiers in Cellular and Infection Microbiology is a leading specialty journal, publishing rigorously peer-reviewed research across all pathogenic microorganisms and their interaction with their hosts. Chief Editor Yousef Abu Kwaik, University of Louisville is supported by an outstanding Editorial Board of international experts. This multidisciplinary open-access journal is at the forefront of disseminating and communicating scientific knowledge and impactful discoveries to researchers, academics, clinicians and the public worldwide. Frontiers in Cellular and Infection Microbiology includes research on bacteria, fungi, parasites, viruses, endosymbionts, prions and all microbial pathogens as well as the microbiota and its effect on health and disease in various hosts. The research approaches include molecular microbiology, cellular microbiology, gene regulation, proteomics, signal transduction, pathogenic evolution, genomics, structural biology, and virulence factors as well as model hosts. Areas of research to counteract infectious agents by the host include the host innate and adaptive immune responses as well as metabolic restrictions to various pathogenic microorganisms, vaccine design and development against various pathogenic microorganisms, and the mechanisms of antibiotic resistance and its countermeasures.