JOURNAL OF PHARMACEUTICAL AND BIOMEDICAL ANALYSIS
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2025
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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 FLUORESCENCE
·
2026
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IF 3.4
Hou Huijing,Luo Mingming,Li Fang,Tan Yijun,Liu Ruowei,Xu Longping,Feng Yanwen,Guo Xiangli,Wu Zijian
Kanamycin (KANA) is a veterinary drug residue that is highly scrutinized in food safety testing. In this study, a metal-organic framework-based aptamer-nanoenzyme (NH 2 -MIL-88B(Fe)/CDs-Apt) was introduced for the dual-mode detection of KANA. NH 2 -MIL-88B(Fe) catalyzes the oxidation of 3,3′,5,5′-tetramethylbenzidine (TMB) by H₂O₂ to form blue ox-TMB, thereby enabling colorimetric detection. As a fluorescence quencher, NH 2 -MIL-88B(Fe) quenches the fluorescence of CDs via photogenerated electron transfer (PET) or fluorescence resonance energy transfer (FRET) mechanisms. The detection limits were 0.716 fM (fluorescent) and 0.709 fM (colorimetric), respectively. The proposed aptasensor was successfully applied to the detection of KANA in eggs, honey, and lake water. This aptasensor demonstrates high sensitivity and accuracy, as well as broad application potential.
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PSYCHOPHARMACOLOGY
·
2026
·
IF 3.3
Chen Yonglan,Lan Yuxin,Yi Jingyan,Qi Xiaoyi,Liu Li,Liu Sha,Xu Xinxin,Liu Huan,He Yufeng,He Bing,Ma Xiaochi,Lü Muhan,Liang Sicheng
Background Many antidepressants exert their effects by modulating the gut microbiota, but it is unknown if this mechanism extends to the tricyclic antidepressant imipramine. Objective We probed the extent to which specific gut bacterial taxa mediate the antidepressant effects of imipramine. Material and methods Using a chronic unpredictable mild stress (CUMS) mouse model, we administered imipramine, the prebiotic inulin, or their combination, and systematically evaluated depressive-like phenotypes. Gut microbial dynamics were profiled by 16S rRNA sequencing, and fecal microbiota transplantation (FMT) was performed to determine the transmissibility of microbiota-derived antidepressant effects. Immunofluorescence staining was used to quantify brain-derived neurotrophic factor (BDNF) expression and to assess intestinal barrier integrity via ZO-1 and occludin. Results Imipramine treatment significantly increased the relative abundances of putative A. muciniphila and L. reuteri , both of which showed strong correlations with behavioral improvements. Furthermore, FMT from imipramine-treated donors effectively alleviated CUMS-induced depressive-like behaviors, upregulated BDNF expression and restored gut barrier integrity in recipient mice. Co-administration of imipramine and inulin produced synergistic antidepressant effects. Conclusions Imipramine partially exerts its antidepressant activity through microbiota modulation, with putative A. muciniphila and L. reuteri emerging as important mediators. The superior efficacy of the imipramine-inulin combination highlights a promising microbiota-targeted strategy for advancing antidepressant therapy.
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JOURNAL OF ETHNOPHARMACOLOGY
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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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Biosensors-Basel
·
2026
·Vol. 16
·期 7
·388
·
IF 6.2
Yaning Liang,Shiyi Fang,Zhuoer Chen,Yuzhuo Chen,Qingqing Yang,Xuelan Shu,Tao Le
Gold nanoparticles (AuNPs) are widely used in aptasensors because of their high extinction coefficient and aggregation-dependent color differences. However, recent studies have indicated that nonspecific interactions between target molecules and AuNPs may dominate the detection signal rather than aptamer–target specific binding. This study systematically investigated the interactions between 13 aminoglycoside antibiotics and AuNPs. We found that all aminoglycoside antibiotics interacted strongly with AuNPs, considerably reducing their salt stability. Furthermore, methoxy polyethylene glycol thiol reversed AuNP aggregation induced by aminoglycoside antibiotics, indicating that it occurs at the secondary minimum. Using density functional theory, we analyzed the molecular structures and charge distribution characteristics of the aminoglycoside antibiotics, elucidating that they replace citrate ions on AuNP surfaces via a ligand exchange mechanism, thereby inducing aggregation. Additionally, both aptamer targets and complementary DNA struggled to desorb the aptamer (KAN6-1) from the AuNP surfaces. Our study demonstrates that the label-free colorimetric assay based on aggregation of unmodified citrate–AuNPs is neither suitable for characterizing the binding affinity of aminoglycoside aptamers nor viable for constructing corresponding colorimetric sensors to detect this class of antibiotics. Thus, researchers should incorporate mechanistic verification and rigorous controls when employing this system to ensure reliable results.
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EUROPEAN JOURNAL OF PHARMACOLOGY
·
2026
·
IF 5.7
Xin Zeng,Yuanmeng Zhao,Bin Deng,Yongning Lu,Huifan Yu,Qiuyun You,Xuejia Zhai
Hypericin alleviates depressive-like behaviors in a rat model of postpartum depression (PPD) by restoring gut microbiota homeostasis and normalizing bile acid metabolism. • Antibiotic-induced gut microbiota ablation abolishes the therapeutic effect of hypericin, demonstrating that gut microbes are essential for its antidepressant action in PPD. • Transcriptomic and metabolomic analyses reveal that hypericin modulates the gut microbiota-bile acid-glucocorticoid signaling axis, identifying this pathway as a PPD-relevant therapeutic target. Background Postpartum depression (PPD) is a mental disorder that occurs in a special period of time, but its pathophysiological mechanism is still unclear. Although hypericin has been shown to have therapeutic effects in previous studies, the underlying mechanisms of its treatment of PPD, especially its interaction with the gut-brain axis, remain to be explored. The aim of this study was to investigate the mechanism of hypericin in the treatment of PPD. Methods The PPD rat model was established by ovariectomy and hormone withdrawal after simulating pregnancy. Postpartum depression-like behavior was assessed by sucrose preference test and open field test. We integrated 16S rRNA sequencing, targeted plasma bile acid metabolomics, brain tissue transcriptomics, histopathology and molecular biology to explain the mechanism. Results Hypericin intervention significantly improved the postpartum depression-like behavior of PPD model rats. This effect was abolished by depletion of the microbiota induced by antibiotic sweeps, thus establishing that the involvement of the gut microbiota is required for the efficacy of hypericin. Hypericin can reverse the abnormal changes of gut microbiota, bile acid metabolism and inflammatory response observed in PPD model, so as to play a role in the treatment of PPD. Conclusion Hypericin plays an antidepressant role in PPD model, mainly by restoring gut microbiota homeostasis, thereby correcting bile acid metabolism disorders. In this study, the “gut microbiota-bile acid” axis is the key pathological feature and therapeutic target of PPD, and hypericin is expected to become a therapeutic candidate based on the gut microbiota. Download: Download high-res image (303KB) Download: Download full-size image
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INTERNATIONAL JOURNAL OF BIOLOGICAL MACROMOLECULES
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2026
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IF 8.7
Junxi Liu,Yan Liu,Yuheng Zheng,Haoyu Wang,Jinglin Wang,Yu Zhang,Kaiping Wang
SCLP remained intact in the stomach and small intestine after oral administration. • SCLP was degraded into oligosaccharide fragments in the cecum and colon. • The intestinal metabolism of SCLP was gut microbiota-dependent. • Phocaeicola vulgatus and Bacteroides uniformis were involved in SCLP metabolism. This study aimed to investigate the intestinal metabolic characteristics and mechanisms of the pectic polysaccharide isolated from the medicinal plant Smilax china L. (SCLP). Firstly, in vitro simulated digestion confirmed that SCLP remained stable in simulated digestive fluids. Subsequently, in vivo real-time tracking of intestinal metabolism based on fluorescent labeling revealed that SCLP maintained its prototype in the small intestine and began to be degraded into fragments (Mw < 4000 Da) upon reaching the cecum and colon, where it was retained for prolonged periods. Pseudo-sterile mouse experiments indicated the mediating role of gut microbiota in SCLP metabolism. Furthermore, metagenomic sequencing suggested that SCLP increased the proportion of polysaccharide utilization loci (PULs) from Phocaeicola vulgatus and Bacteroides uniformis , elevated the gene numbers of carbohydrate-active enzymes (CAZymes) including GHs, GTs and CBMs, and activated pathways of carbohydrate metabolism. Finally, in vitro bacterial culture study verified the degradation and utilization of SCLP by Phocaeicola vulgatus and Bacteroides uniformis . In summary, this work elucidates the intestinal metabolic profile of SCLP, providing valuable insights for its further development and utilization.
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PLoS One
·
2026
·Vol. 21
·期 7
·e0351316
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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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Natural Products and Bioprospecting
·
2026
·Vol. 16
·期 1
·76
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IF 5.8
Li Liang,Zhan Xinyi,Ullah Hidayat,Guo Wenxian,Gui Ping,Peng Weijie,Mei Quanxi,Dai Weibo,Duan Yuting,Yuan Xia,Hu Xianjing
Inflammatory bowel disease (IBD) is a chronic disorder characterized by recurrent intestinal inflammation and gut microbiota dysbiosis. Huanglian-Wendan Decoction (HLWDD) has been clinically used for IBD treatment; however, its underlying mechanisms remain unclear. In this study, a dextran sulfate sodium (DSS, 2.25%)-induced IBD mouse model was established to evaluate the therapeutic effects of HLWDD. The protective mechanisms were investigated in colon tissues of DSS-induced mice using ELISA, immunoblotting, histological, and immunohistochemical analyses. In addition, the impact of HLWDD on gut microbiota dysbiosis was analyzed using 16S rRNA sequencing. Antibiotic treatment was applied before DSS administration to deplete gut microbiota and verify the role of microbial modulation. Furthermore, the phytochemical constituents of HLWDD were characterized using liquid chromatography–quadrupole time-of-flight tandem mass spectrometry (LC-QTOF-MS/MS). The results demonstrated that HLWDD markedly alleviated DSS-induced colitis, as evidenced by reduced body weight loss, rectal bleeding, colon shortening, and disease activity index (DAI) scores. Mechanistically, HLWDD suppressed inflammatory responses in colon tissues by inhibiting the TLR4/MyD88/NF-κB and IL-6/JAK2/STAT3 signaling pathways, while enhancing epithelial barrier integrity through upregulation of ZO-1, Occludin, Claudin-1, and Mucin-2. In addition, HLWDD attenuated endoplasmic reticulum stress (ERS) and apoptosis by downregulating CHOP, phospho-eIF2α, cleaved caspase-3, and Bax, while increasing Bcl-2 expression in colonic tissues. Microbiota analysis revealed an increased abundance of beneficial bacterial genera such as Akkermansia and Escherichia-Shigella –related commensals, along with enrichment of beneficial bacterial families including Ruminococcaceae , Lachnospiraceae , and Verrucomicrobiaceae , whereas potentially harmful taxa such as Escherichia and Paraprevotella were reduced. HLWDD also increased the production of short-chain fatty acids (SCFAs), including acetate, butyrate, and isobutyrate, thereby promoting intestinal homeostasis. Importantly, the protective effects of HLWDD were largely abolished following antibiotic-mediated gut microbiota depletion, confirming the essential role of microbial modulation in its therapeutic action. Collectively, these findings suggest that HLWDD ameliorates IBD by regulating gut microbiota composition and function, thereby inhibiting colonic ER stress and apoptosis and restoring intestinal barrier integrity. This study provides mechanistic evidence supporting the potential clinical application of HLWDD as a novel therapeutic strategy for IBD. Graphical
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MOLECULAR NEUROBIOLOGY
·
2026
·Vol. 63
·期 1
·837
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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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EUROPEAN JOURNAL OF PHARMACOLOGY
·
2026
·
IF 5.7
Xinwen Dong,Zheng Luo,Cuiying Li,Jie Gao,Yue Ma,Xiaoran Ma,Jiahang Yang,Sanqiao Yao,Weidong Wu,Yichun Bai,Qunwei Zhang,Wenjie Ren
Gas explosion (GE) exposure led to significant neuropathology in rats. • GE induced JNK/p38 MAPK pathway activation, ferroptosis, and inflammation. • Sodium butyrate mitigated these effects by inhibiting JNK/p38 MAPK activation. This study investigated the neuroprotective effects of sodium butyrate (NaB) against gas explosion (GE)-induced traumatic brain injury (TBI), with particular emphasis on its modulation of ferroptosis. GE exposure was simulated using a shock tube in vivo and a shockwave therapy instrument in vitro . A comprehensive assessment was performed, including behavioral tests, histopathological examination, molecular analyses (c-Jun N-terminal kinase (JNK)/p38 mitogen-activated protein kinase (p38 MAPK), solute carrier family 7 member 11 (SLC7A11)/glutathione peroxidase 4 (GPX4), and interleukin-6 (IL-6)/interleukin-10 (IL-10)/tumor necrosis factor-α (TNF-α)), and in vitro validation using a CTX TNA2 rat astrocyte/H19-7 rat hippocampal neuron/GMI-R1 rat microglia (CTX/H19-7/GMI-R) tri-culture system. Pharmacological inhibition with SP600125 (a JNK inhibitor), SB203580 (a p38 MAPK inhibitor), and ferrostatin-1 (Fer-1, a ferroptosis inhibitor) was employed to confirm pathway involvement. GE exposure induced profound neuropathological changes, characterized by mitochondrial cristae disruption, inflammatory cell infiltration, and locomotor deficits. At the molecular level, GE exposure activated the JNK/p38 MAPK pathway (as evidenced by increased JNK and p38 phosphorylation), triggered ferroptosis (elevated Fe 2+ and malondialdehyde levels, with reduced GPX4 and SLC7A11 expression), and elicited a pro-inflammatory response (increased IL-6 and TNF-α, decreased IL-10). NaB administration effectively counteracted these deleterious effects by restoring redox homeostasis, suppressing JNK/p38 activation, and rebalancing inflammatory cytokine profiles. Notably, co-administration of pathway inhibitors potentiated the protective effects of NaB, further corroborating the involvement of JNK/p38 MAPK-mediated ferroptosis in GE-induced TBI. Collectively, these findings indicate that NaB attenuates GE-induced TBI and ferroptosis, likely through inhibition of the JNK/p38 MAPK signaling pathway. Download: Download high-res image (288KB) Download: Download full-size image
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