JOURNAL OF PHARMACEUTICAL AND BIOMEDICAL ANALYSIS
·
2025
·
IF 3.1
Junling Li,Qianru Gao,Hongtao Liu,Songlin Liu,Yanchun Wang,Xiongjie Sun,Junping Zheng,Huabing Yang,Baifei Hu
Xiexin Tang (XXT) is a classic Chinese medicine formula that can be used to treat Atherosclerosis (AS). This study aimed to investigate the mechanism by which XXT regulated AS lipid levels. Firstly, the mixture components of XXT were analyzed by High-performance liquid chromatography-tandem mass spectrometry (HPLC-MS/MS). Then, the AS model based on Apolipoprotein E knockout (ApoE -/- ) mice was established. Cytokines related to lipid metabolism and bile acid metabolism were detected by Quantitative Real-time PCR (qRT-PCR). 16S rDNA gene sequencing was performed to analyze differential bacterial populations, and the mechanism of XXT regulation of bile acids affecting lipid metabolism was further explored by targeted metabolomics. Further, antibiotic-treated mice were used to investigate the role of gut microbiota in the anti-AS effect of XXT. The results showed that XXT attenuated the lipid levels and reversed the abnormal elevation of cytokines, such as hepatic lipid metabolism and inflammatory reaction in AS mice. XXT also repaired the gut barrier damage and reversed gut microbiota disorders in AS mice. Furthermore, the metabolic levels of bile acids were reshaped by XXT. Whereas, in the absence of gut microbiota, XXT failed to attenuate lipid levels and inhibit the expression of cytokines related to inflammation and bile acid metabolism in AS mice and failed to play a role in ultimately treating AS. In conclusion, XXT could effectively inhibit the inflammatory reaction and lipid accumulation in AS mice, and this effect was closely related to its remodeling of gut microbiota to regulate bile acid metabolism.
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JOURNAL OF ETHNOPHARMACOLOGY
·
2026
·
IF 6.8
Huan-qing Gao,Ning Zhang,Ge-ning Li,Li Wen,Yao Li,Min Li,Tai-wei Dong,Lian Zhong,Da-neng Wei,Meng-meng Zhang,Li Ou
Ethnopharmacological relevance Da- Jian-Zhong decoction (DJZD), a Chinese medicinal formula, exhibits therapeutic effects in the clinical management of diarrhea-predominant irritable bowel syndrome (IBS-D). Accumulating studies have demonstrated that DJZD can regulate the gut-brain balance in IBS-D model rats; however, its underlying molecular mechanism remains unclear. Aim of the study To explore the potential mechanism by which DJZD restores the gut-brain axis in IBS-D model rats. Materials and methods Firstly, the therapeutic effects of DJZD in IBS-D model rats were evaluated based on the Bristol stool scale, abdominal withdrawal reflex (AWR) score, open field test (OFT) behavior, intestinal barrier integrity, and brain-gut peptide levels. Moreover, alterations in gut microbiota was detected using sequencing of the whole microbial genome. Subsequently, fecal microbiota transplantation (FMT) was performed to explore whether the regulatory effect of DJZD on the gut-brain axis against IBS-D was dependent on gut microbiota. The UHPLC-QTRAP-MS/MS was utilized to analyze bile acids (BAs) profiles and identify gut microbiota-derived BAs metabolites responsible for the beneficial effects of DJZD. Finally, the role of BAs metabolites in restoring the gut-brain axis was further verified using the IBS-D model rats. Results Treatment with DJZD not only decreased AWR score, improved stool score and intestinal barrier integrity, but also enhanced sucrose preference and changed OFT performance of IBS-D rats. Meanwhile, DJZD normalized the levels of 5-hydroxytryptamine (5-HT) and substance P (SP) in both the colon and hippocampus. Fecal microbiota harvested from DJZD-treated rats also reversed these IBS-D-associated pathological manifestations. Moreover, DJZD notably elevated the levels of secondary BAs (SBAs) in colonic contents of IBS-D rats, particularly norchenodeoxycholic acid (NorDCA), lithocholic acid (LCA), deoxycholic acid (DCA), and 3β-ursodeoxycholic acid (3β-UDCA). The elevated SBAs were positively correlated with the relative abundances of Akkermansia sp., Ruminococcus sp., and Clostridium sp. This could be attributed to the ability of these bacteria to produce bile salt hydrolases (BSH) and 7α-hydroxysteroid dehydrogenases (7α-HSDH). Additionally, administration of an LCA and DCA mixture was found to improve intestinal and brain dysfunction and restored abnormal 5-HT and SP levels in IBS-D rats. Conclusion DJZD restores gut-brain balance in IBS-D rats by regulating gut microbiota-bile acid axis, which provides a promising therapeutic strategy for IBS-D via targeting bile acid metabolites and intestinal bacteria.
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Advanced Science
·
2026
·
IF 14.1
Kaikai Zhang,Yuchuan Chen,Jiayuan Wan,Jianzheng Yang,Lijian Chen,Qingyuan Li,Anding Zhou,Nian Zhou,Jiuyang Ding,Qi Wang,Jian Sun
Nanoplastics (NPs) exposure can cause severe hepatic injuries. Gut microbiota is considered a contributing factor to multiple hepatic injuries. However, its role in NPs‐induced hepatic injuries remains unclear, and microbial intervention strategies are required. Our results reveal that oral exposure to polystyrene NPs reduces gut probiotic Bifidobacterium pseudolongum ( B.p ) and its metabolite inosine. Gut microbiota from NPs‐administered mice partially reproduces NPs‐related impairment of gut homeostasis and hepatic injury in recipient mice. Moreover, B.p colonization improves NPs‐induced gut homeostasis impairment and hepatic injury, and its protective effects are reproduced by supplementation with inosine. Mechanically, B.p colonization increases hepatic level of inosine and subsequently normalizes the expression of its target A2AR. Meanwhile, increased inosine inhibits the miR155/SOCS1/NF‐κB pathway and represses NPs‐induced M1 macrophage polarization. CGS21680 , an agonist of A2AR, effectively represses lipopolysaccharide (LPS)‐induced M1 macrophage polarization and inhibits the miR155/SOCS1/NF‐κB pathway in vitro. Further, miR155 knockout inhibits NPs‐induced M1 macrophage polarization, but does not influence the suppression of NPs on A2AR. These findings suggest that B.p ‐derived inosine can repress NPs‐induced M1 macrophages polarization by inhibiting the miR155/SOCS1/NF‐κB pathway via targeting A2AR. Altogether, this study further clarifies the role of gut microbiota in NPs‐induced hepatic injury and provides a potential microbial therapeutic strategy. Probiotic B.p colonization elevated gut‐derived inosine level in the liver, while elevated inosine activated A2AR and subsequently blocked NPs‐induced polarization of M1 macrophages by repressing the miR155/SOCS1/NF‐κB pathway. This reduced the release of inflammatory cytokines and thereby, mitigated NPs‐induced hepatic injury.
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Microorganisms
·
2026
·Vol. 14
·期 7
·1592
·
IF 4.7
Yufan Wu,Xiaoqiang Huang,Qiang Gu,Yun Li,Yuan Zhou,Lu Sun,Xiang Wang
Clustered regularly interspaced short palindromic repeats (CRISPR) are widespread in bacterial and archaeal genomes as an adaptive immune system against invading mobile genetic elements. This study investigated the distribution of CRISPR loci and their potential association with antimicrobial resistance (AMR) in 40 foodborneListeria monocytogenesisolates. CRISPR analysis showed that 18 isolates harbored CRISPR Locus 1, five carried Locus 2, and five possessed both loci. Antimicrobial susceptibility testing against seven antimicrobial agents indicated that most isolates were highly susceptible to the tested agents. Specifically, all isolates were susceptible to gentamicin, ampicillin, penicillin, and tetracycline, whereas resistance was observed in a small subset of isolates: four were resistant to chloramphenicol, five to levofloxacin, and four to ciprofloxacin. Statistical analysis showed no statistically significant association between the presence of CRISPR loci and antimicrobial susceptibility phenotypes. These findings provide baseline information on CRISPR locus distribution and antimicrobial susceptibility profiles in foodborneL. monocytogenesisolates. Further studies based on larger isolate collections, whole-genome sequencing, and characterization of associatedcasgenes are needed to clarify the potential role of CRISPR-Cas systems in AMR evolution in this species.
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PLoS One
·
2026
·Vol. 21
·期 7
·e0351316
·
IF 2.8
Xiongbao Zhang,Yating Fu,Jiahui Chen,Hao Shen,Yumeng Du,Jun Wu,Hongjing Lai,Yu Liu,Jingbo Chen,Xiaomei Hou,Wenjun Chang,Xuefei Hu
Background
The gut microbiota is closely related to exercise, but the interrelationship between the two remains elusive. In this study, we aimed to explore differences in the gut microbiota between young adults with exercise and sedentary lifestyles. In addition, we evaluated the effects of gut microbiota from these different lifestyle populations on endurance exercise capacity.
Methods
The exercise status and nutritional characteristics of young adults were evaluated by PARS-3 and food frequency questionnaires. The gut microbiota of young adults from exercise and sedentary lifestyle groups was analyzed by 16S rRNA analysis. Subsequently, we performed fecal bacteria transplantation (FMT) from the human donors into mice and evaluated the effects on their endurance exercise capacity.
Results
The exercise group exhibited significantly higher gut microbiota diversity compared to the sedentary group. Several beneficial bacteria, including Veillonella, Faecalibacterium, and Bacteroides, were enriched in the exercise group. The FMT experiment confirmed that mice receiving microbiota from the exercise group showed significantly improved endurance exercise capacity.
Conclusion
Young people who exercise regularly possess a more diverse gut microbiota enriched with beneficial bacteria. This exercise-associated microbiota has the potential to directly improve exercise capacity.
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MOLECULAR NEUROBIOLOGY
·
2026
·Vol. 63
·期 1
·837
·
IF 5.5
Wang Yan,Yuan Bin,Li Yunzi,Sun Yan,Xie Yi,Cheng Hao,Zhang Yao,Wu Qi,Tang Jun
Neuropathic pain (NP) presents a significant challenge for patients with chronic diseases, characterized by spontaneous pain and hyperalgesia, with recent studies highlighting the involvement of the gut microbiota in its pathogenesis. Increasing evidence suggests that melatonin mitigates systemic inflammation and remodels gut microbiota. The present study further explored the mechanism by which oral melatonin ameliorates pain-related behavior following peripheral nerve injury. In this study, mice with chronic constriction injury (CCI) were orally administered melatonin (100 mg/kg) for 14 days. Pain behaviors were evaluated using mechanical allodynia and thermal hyperalgesia tests. Gut microbiota profiles were assessed via 16S rRNA sequencing, and microbiota-dependent effects were verified through antibiotic treatment (ABX) and fecal microbiota transplantation (FMT). Linoleic acid (LA) levels in serum and spinal cord were measured using liquid chromatography–mass spectrometry (LC–MS), and protein expression of NLRP3, caspase-1, and GSDMD in spinal cord tissue was examined by immunoblotting. Melatonin treatment significantly increased the mechanical pain threshold and prolonged thermal withdrawal latency in CCI mice. It also remodeled the dysbiotic gut microbiota, and these protective effects were abolished by antibiotic treatment but restored by FMT. Protein analysis revealed upregulation of NLRP3 and GSDMD in CCI mice, both of which were suppressed following melatonin administration. Moreover, melatonin-induced microbiota modulation elevated LA levels in serum and spinal cord. Supplementation with LA alone alleviated NP and inhibited NLRP3, caspase-1, and GSDMD activation. These findings suggest that oral melatonin treatment effectively ameliorates NP in CCI mice associated with the neuroinflammation and microbiota-metabolites-brain axis.
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JOURNAL OF CHROMATOGRAPHY B-ANALYTICAL TECHNOLOGIES IN THE BIOMEDICAL AND LIFE SCIENCES
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2026
·
IF 2.5
Jia-Hui Gong,Jun-Jun Wang,Ming-Xia Lu,Yang Lin,Qing You,Hui-Zhi Luo,Qian-Hua Yan,Jiang-Yi Yu,Jian-Dong Zou,Chang-Yin Li
Multi-omics reveals the metabolic impact of Qikui granules on db/db mice. • Gut microbiota is essential for Qikui granules to exert anti-DKD effects. • Candidatus Arthromitus mediates the anti-DKD effect of Qikui granules. Diabetic kidney disease (DKD) has a complex and multifactorial pathogenesis, and highly effective pharmacotherapies for this condition remain limited. Qikui granules (QKG), a compound traditional Chinese medicine preparation, has shown favorable therapeutic efficacy against DKD in clinical studies. Our prior work, based on integrated network pharmacology, 16S rRNA gene sequencing, and lipidomic profiling of serum and kidney tissues, demonstrated that QKG ameliorates DKD in db/db mice by enriching Candidatus Arthromitus and modulating lipid homeostasis. As a follow-up validation of our earlier findings, the present study adopts an integrated multi-omics strategy combining fecal metabolomics, lipidomics, and 16S rRNA sequencing, coupled with a pseudo-germ-free mouse model, to further elucidate the therapeutic efficacy of QKG against DKD and the pivotal role of gut microbiota in its renoprotective effects. Firstly, fecal metabolomic and lipidomic profiling was performed to explore the pharmacological mechanisms of QKG against DKD. Subsequently, a pseudo-germ-free mouse model established via antibiotic administration was used to verify the microbiota-mediated mechanism of QKG. Metabolomic and lipidomic analysis revealed that QKG significantly reversed the upregulation of 24 special potential biomarkers (SPBs) in feces, including phosphatidylcholines (PC), phosphatidylethanolamines (PE) and unsaturated fatty acids (UFA); glycerophospholipid metabolism and arachidonic acid metabolism were identified as the most relevant pathways. The pseudo-germ-free mouse model validated the microbiota-dependent therapeutic effect of QKG on DKD from both pharmacodynamic and gut microbiota composition perspectives. Furthermore, correlation analysis showed that the 24 SPBs associated with the anti-DKD efficacy of QKG were negatively correlated with the relative abundance of Candidatus Arthromitus. Collectively, our findings suggest that QKG exerts microbiota-dependent efficacy against DKD-related metabolic disorders and inflammation, mainly by increasing the abundance of Candidatus Arthromitus and thereby reducing the levels of PC, PE, and UFA. Download: Download high-res image (201KB) Download: Download full-size image
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FOOD RESEARCH INTERNATIONAL
·
2026
·
IF 8.8
Yushi Li,Jinmei Li,Jiteng Deng,Pei Xia,Guicheng Zhou,Zhenjun Zhu,Yu Ding,Jingge Yang,Fen Zhang
Phocaeicola vulgatus -centered network and ornithine synthesis are impaired in obese individuals. • P. vulgatus alleviates HFD-induced obesity in humanized rats. • P. vulgatus shows a potential functional association with Phascolarctobacterium faecium in enhancing arginine biosynthesis. • Elevated systemic arginine is associated with activated host hepatic retinoic acid signaling. • The arginine-retinoic acid axis highlights P. vulgatus as a probiotic target. Fecal microbiota transplantation (FMT) shows inconsistent clinical efficacy in treating obesity, and the specific microbial determinants dictating its success remain poorly characterized. Our previous clinical FMT trial identified Phocaeicola vulgatus as a key microbe contributing to the therapeutic efficacy of obesity treatment. Here, to investigate its role in obesity, we established an independent clinical cohort comprising obese and lean individuals, revealing that the P. vulgatus -centered network and ornithine synthesis are impaired in the obese group. We then confirmed causality by utilizing a humanized rat model carrying microbiota from a P. vulgatus -deficient obese patient, demonstrating that P. vulgatus supplementation significantly mitigates HFD-induced obesity, including reductions in body weight and serum total cholesterol levels, as well as the alleviation of hepatic steatosis. To further explore the functional mechanisms of P. vulgatus , integrated metagenomic and metabolomic analyses revealed a potential functional association between P. vulgatus and Phascolarctobacterium faecium that is associated with enhanced intestinal arginine biosynthesis and systemic availability. Furthermore, hepatic transcriptomics linked these elevated circulating arginine levels to the upregulation of retinoic acid (RA) signaling. Taken together, our findings outline a potential microbial-host network wherein P. vulgatus mitigates obesity via the arginine-RA axis, providing a valuable scientific basis for exploring this strain as a probiotic candidate for metabolic health. Download: Download high-res image (165KB) Download: Download full-size image
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IMMUNOLOGY
·
2026
·
IF 5.4
Sisi Zhang,Zhou Jingxiang,Caixia Tan,Yuanyuan Xiao,Ju Zou,Biyue Tian,Anhua Wu,Chunhui Li
Clostridioides difficile infection (CDI) remains a major cause of antibiotic-associated colitis and is characterized by excessive intestinal inflammation, epithelial barrier disruption and impaired mucosal repair. Although sodium butyrate (NaB), a microbiota-derived short-chain fatty acid, has demonstrated anti-inflammatory and barrier-protective properties, the immunological mechanisms underlying its protective effects during CDI remain incompletely understood. In this study, we investigated the role of NaB in regulating macrophage polarization and epithelial repair using murine CDI models, primary bone marrow-derived macrophages, THP-1-derived macrophages, Caco-2 epithelial cells and macrophage–epithelial co-culture systems. NaB treatment significantly alleviated CDI-associated weight loss, colonic shortening, histopathological injury and inflammatory cytokine production while restoring epithelial barrier integrity and tight junction protein expression. Mechanistically, NaB promoted macrophage polarization towards an anti-inflammatory M2 phenotype, characterized by increased CD206 and IL-10 expression and reduced CD86 and IL-1β expression. These immunomodulatory effects were accompanied by suppression of PI3K/Akt/mTOR signalling in both colonic tissues and macrophages. Pharmacological inhibition and activation studies further supported the involvement of this pathway in NaB-mediated macrophage reprogramming. Importantly, conditioned medium from NaB-treated macrophages enhanced epithelial viability, migration and barrier-associated protein expression, whereas IL-10 neutralization partially abolished these protective effects, highlighting a critical role for macrophage–epithelial crosstalk. Collectively, our findings demonstrate that low-dose NaB protects against CDI-induced intestinal injury through coordinated regulation of macrophage polarization and epithelial barrier repair, at least in part via modulation of PI3K/Akt/mTOR signalling. These results identify NaB as a promising host-directed therapeutic strategy for CDI and provide new insights into microbiota-derived metabolite–immune interactions during intestinal inflammation.
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CHEMICAL ENGINEERING JOURNAL
·
2026
·
IF 12.5
Pengyu Hu,Longwen Lei,Chenglong Fu,Yi Wang,Haiming Li,Xing Wang,Zhiwei Wang,Lan Yao,Yanzhu Guo
Lignin-based CDs with fluorescence and oxidase-like activity were designed firstly • Synergistic engineering of rich graphitic N and large sp 2 domains narrows bandgap • Relationship of structure and visible light-driven oxidase-like activity was revealed • A ratiometric colorimetric/fluorescent system for nitrite detection was constructed Renewable lignin-derived carbon dots with oxidase activity are potential sustainable alternatives for natural enzymes, but their weak visible-light absorption fundamentally inhibits triggering their oxidase-like activity. Herein, we successfully engineered N-doped lignin carbon dots (LCD MA ) with superior visible-light harvesting capacity via enlarging their conjugated sp 2 domain size and graphitic N content. Owing to the synergistic effect of these structures, the bandgap of LCD MA was narrowed to 3.241 eV, which efficiently extended its visible absorption range to 500 nm, and red-shifted its fluorescent light to green region. The superior visible absorption endowed LCD MA with outstanding oxidase-like activity via boosting the generation of photogenerated electrons, which drove the reduction of O 2 to • O 2 − . The LCD MA exhibited a rapid catalytic rate (V max = 21.64 × 10 −5 mM s −1 ) and strong affinity (K m = 0.70 mM) for 3,3′,5,5′-tetramethylbenzidine. Owing to the catalytic activity and green fluorescence of LCD MA , we constructed a ratio-metric colorimetric and fluorescence dual-mode solution system for nitrite detection in the linear range of 2–250 μM, whose detection limits were as low as 0.85 μM and 1.60 μM, respectively. Furthermore, we engineered an all-in-one portable sensing platform by encapsulating LCD MA and TMB into hydrogel for visual and quantitative detection of nitrite through smartphone with a detection limit of 8.95 μM. This study not only provided an effective strategy for rationally engineering sustainable carbon dots with oxidase-like activity from renewable biomass, but also delivered a practical and effective analytical tool for food safety monitoring. Download: Download high-res image (370KB) Download: Download full-size image
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APPLIED AND ENVIRONMENTAL MICROBIOLOGY
·
2026
·
IF 4.2
Haiqin Meng,Shun Pan,Zening Chai,Lixiang Zhou,Tianyu Zheng,Hanyu Zhang,He Fu,Lei Zou,Dongqi Liu,Jingcheng Dai,Dazhong Yan,Hong-Jun Chao
The catabolism of the priority environmental pollutant 2,4-xylenol requires bacteria to oxidize its ortho-methyl group. Its exact biochemical mechanism is uncharacterized until now. In this study, we resolve key metabolic bottlenecks in Pseudomonas putida NCIMB 9866. We demonstrate that functionally redundant Rieske oxygenase systems ensure the robust ortho-methyl oxidation of 2,4-xylenol. On the para-methyl oxidation branch, PchA2 acts as the main aldehyde dehydrogenase. It shows significantly higher catalytic efficiency than the previously reported PchA. Additionally, we characterized PmmA1B1, a newly identified three-component Rieske oxygenase system responsible for ortho-methyl oxidation, which is supported by two redundant isoenzymes (PmmA2B2 and PmmA3B3), by recruiting the shared endogenous ferredoxin Orf05169. The PmmA1B1-Orf05169 system catalyzes the successive oxidation of the ortho-methyl group of 4-hydroxy-3-methylbenzoate to a carboxyl group, yielding the high-value pharmaceutical precursor 4-hydroxyisophthalate. Structural and kinetic data revealed that the active site architecture of PmmA1 enables efficient successive oxidation, distinguishing it from isoenzymes PmmA2B2 and PmmA3B3 that, when coupled with Orf05169, catalyze only incomplete oxidation. Overall, these results complete the 2,4-xylenol catabolic pathway by defining the enzymes required for both para- and ortho-methyl oxidation. They also reveal functional redundancy as an adaptive feature of microbial aromatic degradation and establish Rieske oxygenases as biocatalysts for converting methylated aromatic pollutants into value-added chemicals.
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Cell Host & Microbe
·
2026
·
IF 23.2
Fengqing Lin,Lianglan Li,Yuanpeng He,Shujie Xu,Qiufen Mo,Wangsen Cao,Aikun Fu,Weiqin Li
The enteric microbiome and nutrient sensing within the small intestine play critical roles in maintaining host metabolic homeostasis. Although various bacteria and some fungi have established functions in nutrient metabolism, the role of the enteric virome remains poorly understood. Here, we demonstrate that the enteric virome significantly influences carbohydrate digestion and absorption independently of the bacteriome. Furthermore, the virome elicits distinct responses across different intestinal cell types. Specifically, it activates programs for carbohydrate digestion and absorption in intestinal epithelial cells while simultaneously stimulating antigen-presenting cells―Th17 cells―to produce interleukin-22, a cytokine that curbs excessive carbohydrate uptake. The virome’s effect on carbohydrate digestion and absorption—whether suppressive or stimulatory—depends on the presence or absence of immune surveillance. This intricate interplay between metabolic and immune pathways establishes the enteric virome as a pivotal regulator of metabolism and reveals the virome’s intrinsic capacity to autonomously modulate vertebrate intestinal physiology.
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危险品化学品经营许可证（带存储）