FOOD RESEARCH INTERNATIONAL
·
2024
·
IF 7
Bing Zheng,Tianxiang Ao,Xiaole Zhao,Yi Chen,Jianhua Xie,Xingcai Gao,Li Liu,Xiaobo Hu,Qiang Yu
The impact of different forms of dietary fiber (total, insoluble or soluble) derived from the same source on health remains incompletely understood. In this study, the effects of total, insoluble, and soluble dietary fiber extracted from highland barley (HDF, HIDF, and HSDF) on combating obesity were evaluated and compared. A high-fat diet (HFD) was used to induce obesity in a murine model, followed by gavage administration of HDF, HIDF, or HSDF, and a comprehensive multi-omics approach was utilized to assess and compare the effects of these dietary fibers on obesity-related parameters. The results showed that all three dietary fibers significantly reduced body weight, modified blood lipid profiles, and ameliorated tissue damage in HFD-fed mice. Additionally, 16S rRNA sequencing analysis of mice feces showed that three types of dietary fiber exerted varying degrees of impact on the composition and abundance of gut microbiota while simultaneously promoting the biosynthesis of short-chain fatty acids. Specifically, HDF supplementation remarkably enhanced the abundance of Coprococcus , while HIDF and HSDF supplementation elevated the levels of Akkermansia and Allobaculum , respectively. Transcriptomic and proteomic results suggested the PPAR signaling pathway as a central regulatory mechanism influenced by these fibers. HDF and HIDF were particularly effective in modulating biological processes related to triglyceride and fatty acid metabolism, identifying Abcc3 and Dapk1 as potential targets. Conversely, HSDF primarily affected processes related to membrane lipids, ceramides, and phospholipids metabolism, with Pck1 identified as a potential target. Collectively, HDF, HIDF, and HSDF demonstrated distinct mechanisms in exerting exceptional anti-obesity properties. These insights may inform the development of personalized dietary interventions for obesity.
研究领域:
营养学
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分子生物学
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微生物学
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PubMed
高影响因子
Journal of Future Foods
·
2025
·
IF 7.2
Haohao Tang,Luyi Wang,Wanqiang Sun,Guocheng Du,Jingwen Zhou,Jian Chen,Xin Guan
Cultured meat provides a sustainable and safe alternative to traditional meat production by culturing animal cells in vitro . Cultured fat is an important component of cultured meat, contributing to its flavor, texture, and nutrition. Induced adipogenic differentiation is the most important step in the production of cultured fat, but conventional adipogenic inducer cocktails are complex and contain non-food-grade substances, which introduces a food safety risk for cultured meat products. Here we demonstrated that a food-grade substance, peanut oil (P-OIL), promoted adipogenic differentiation and lipid accumulation of bovine adipose-derived stem cells (bADSCs), based on which a simple and efficient approach was developed to produce cultured bovine fat. Mechanistic analysis showed that P-OIL upregulated genes involved in lipid synthesis and storage, such as PPARγ, CPT2 , and LPL , by activating the PPAR signaling pathway during adipogenesis. Notably, the lipid composition of cultured bovine fats generated using P-OIL induction was similar to that of fats obtained from farmed cattle, but free of trans -fatty acids. This study provides valuable insights into the production of safe, healthy, and nutritious cultured fats.
研究领域:
生物工程
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食品科学
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细胞生物学
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DOI
高影响因子
Advanced Science
·
2026
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IF 14.1
Mingquan Gao,Xudong Yu,Ziqian Shang,Mengyao Tan,Xie Huang,Zaizhi Du,Xiaojiao Wang,Xinrui Yang,Ximei Luo,Weidong Wang,Rong Li,Shenglin Luo
Radiation‐induced lung injury (RILI) is a major complication of nuclear radiation exposure and thoracic radiotherapy, driven in part by a vicious cycle of oxidative stress and mitochondrial dysfunction. Peroxisome proliferator‐activated receptor gamma (PPAR‐γ), a key regulator of mitochondrial homeostasis and inflammatory resolution, therefore represents a potential therapeutic target, yet multi‐omics analyses revealed that this immunometabolic checkpoint remains functionally constrained in irradiated macrophages. To reactivate this pathway, we developed an inhalable, ROS‐responsive nanospray (HANP) by loading nicotinamide adenine dinucleotide (NAD + ) and astaxanthin (ASX) into a hollow mesoporous polydopamine (HMPDA) shell. Excess ROS in microenvironment triggers oxidative degradation of the HMPDA shell, enabling intracellular release of NAD + and ASX. Mechanistically, NAD + promotes SIRT1‐mediated deacetylation of PPAR‐γ, whereas ASX serves as an activating ligand, thereby cooperatively restoring PPAR‐γ signaling. This response re‐establishes macrophage mitochondrial homeostasis by coordinating mitochondrial biogenesis and mitophagy, which subsequently promotes a shift toward a reparative macrophage phenotype. In murine models of focal thoracic irradiation and lethal whole‐body irradiation, HANP markedly attenuated lung injury and improved survival. Collectively, these findings identify macrophage PPAR‐γ as a therapeutically actionable redox‐immunometabolic regulator and support inhaled dual‐activation of this pathway as a promising strategy for protection against RILI in both clinical and emergency settings. A nebulized nanoassembly alleviates radiation‐induced lung injury by reprogramming macrophages through coordinated ROS scavenging, NAD + replenishment, and PPAR‐γ activation. Redox balance, mitochondrial homeostasis, and immune regulation are restored, revealing a microenvironment‐centered strategy for localized radioprotection.
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高影响因子
Food & Function
·
2026
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IF 6.3
Ziyuan Zhou,Xiaxia Pan,Jiali Ni,Zhuoqi Lou,Yangfan Shen,Shiman Jiang,Xiangmin Dong,Fengjiao Wang,Yanfei Chen,Lanjuan Li
Existing evidence indicates that pre-existing metabolic dysfunction-associated steatotic liver disease (MASLD) confers susceptibility to acute liver injury (ALI). Nevertheless, the underlying mechanism prompting ALI risk in such condition is not fully uncovered yet. Gut dysbiosis has been well-documented in MASLD patients which prompts us to hypothesize that gut dysbiosis may serve as a contributing factor and regulating target to ALI susceptibility. A case-control study was performed and verified the increased risk of ALI in MASLD patients. Mice pretreated with MASLD mice/patients-derived fecal microbiota transplantation (FMT), demonstrated worsened ALI after D-GalN/LPS injection. We identified significant gut dysbiosis with decreased microbial α-diversity, beneficial genus lactobacillus, increased potential harmful bacteria Campylobacter and helicobacter. Probiotic Akkermansia muciniphila (A. muciniphila) was reported to improve gut dysbiosis. Thus, we tested the effect of A. muciniphila on ALI mice pretreated with MASLD mice-derived FMT. A. muciniphila significantly ameliorated the worsened ALI and improved gut dysbiosis. Transcriptomic analysis reveled that A. muciniphila restored the impaired liver PPAR-α signaling, alleviating the aggravated NF-κB signaling and downstream inflammation response in liver. Specifically, A. muciniphila restored the decreased abundance of PPAR-α agonist daidzein in colon, thereby restoring PPAR-α activation and inhibiting NF-κB signaling in liver. Daidzein is also capable to ameliorate ALI aggravated by MASLD-associated dysbiosis, accompanied by PPAR-α activation and NF-κB inhibition. Our findings revealed that gut dysbiosis in MASLD increased the risk of ALI. A. muciniphila exhibited preventive potential for MASLD patients to reduce ALI risk. Daidzein/PPAR-α/NF-κB signaling is important to maintain host resistance to hepatoxic challenge.
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高影响因子
ECOTOXICOLOGY AND ENVIRONMENTAL SAFETY
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2025
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IF 6.1
Jinping Fan,Yang Geng,Jinglei Liu,Qixin Huang,Jie Zeng,Huiyuan Cao,Xiaokai Lu,Hao Cheng,Zhili Qi
Deoxynivalenol (DON), a pervasive mycotoxin contaminating crops and soil, poses significant threats to ecological security and intestinal homeostasis. While gut microbiota dysbiosis is implicated in DON-induced enterotoxicity, the engineering-driven mechanisms linking gut-derived extracellular vesicles (EVs) to environmental-host interactions remain unexplored. Here, we isolated and characterized gut-derived EVs (DON-EVs) from DON-exposed mice, employing ultracentrifugation, transmission electron microscope, nanoparticle tracking analysis, and protein marker validation. Functional validation demonstrated that DON-EVs potently attenuated M2 macrophage polarization and downregulated tight junction proteins, thereby exacerbating intestinal barrier dysfunction. miRNA-seq revealed 8 differentially expressed miRNAs in DON-EVs, with 5_19616 exhibiting pronounced pro-inflammatory effects via screening and inhibitor assays. Mechanistically, 5_19616 suppressed peroxisome proliferator-activated receptor gamma (PPAR-γ) expression through direct targeting, inhibiting M2 macrophage polarization and downregulating tight junction proteins, thereby compromising intestinal barrier integrity. Adoptive transfer of 5_19616-transfected macrophages into mice induced systemic inflammation, epithelial damage, and PPAR-γ pathway inhibition, mirroring DON-induced pathology. Crucially, our findings highlight EVs as nanoscale bioengineering vectors mediating environmental-host crosstalk. Collectively, this study pioneers the "gut-EVs-miRNA-macrophage" axis as a novel engineering target, offering miRNA-directed strategies to mitigate mycotoxin-related diseases, with potential applications in nanomedicine and environmental health engineering.
研究领域:
毒理学
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免疫学
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分子生物学
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环境卫生
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纳米医学
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胃肠病学
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PubMed
高影响因子
Virulence
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2026
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IF 5.4
Kun Yan,Xiuling Wang,Zongyi Bo,Chengcheng Zhang,Mengjiao Guo,Xiaorong Zhang,Yantao Wu
Avian infectious bronchitis virus (IBV) belongs to the genus Gammacoronavirus (family Coronaviridae), causes severe multi-system disease in chickens, inflicting major global economic losses. The molecular interplay between IBV and host metabolic networks remains poorly understood. Through integrated transcriptomic, metabolomic, and lipidomic profiling of oviduct tissues from specific-pathogen-free (SPF) chickens infected with the IBV QXL strain, we demonstrate tripartite metabolic reprogramming: 1) redirected glucose flux through the pentose phosphate pathway (PPP) to fuel nucleotide synthesis, 2) rewired lipid metabolism to prioritize de novo membrane biogenesis over fatty acid β-oxidation, and 3) orchestrated glycerophospholipid remodeling. This integrated analysis revealed a coordinated upregulation of fatty-acid biosynthesis genes and accumulation of specific glycerophospholipids and eicosanoids. Mechanistically, IBV co-opts the Warburg effect and PPP activation while uniquely suppressing fatty acid β-oxidation to channel fatty acids toward lipid droplets (LDs) biogenesis. Phosphatidylserine (PS) overproduction (e.g. 2.55-fold increase in PS(22:0/22:6)) and phospholipase A2 (PLA2)-mediated lysophospholipids (Lyso-PLs) and eicosanoids generation (e.g. 7.09-fold increase in prostaglandin E2 (PGE2)) emerged as critical regulators of membrane dynamics and inflammatory signaling. This process was centrally coordinated by the significant activation of peroxisome proliferator-activated receptor (PPAR) (e.g. 1.74-fold increase in ACSL1) and transforming growth factor-beta (TGF-β) (e.g. significant increase in p-SMAD2) signaling pathways, directly linking lipid remodeling to immunomodulation. Functionally, targeting acetyl-CoA carboxylase (ACC) or glucose-6-phosphate dehydrogenase (G6PD), alongside TGF-β pathway modulation, synergistically curtailed viral replication in vitro. Our findings delineate a critical PPAR-TGF-β cross-talk that governs lipid remodeling during infection and identify host metabolic nodes that are potentially targetable for antiviral intervention.
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PubMed
高影响因子
MOLECULES
·
2022
·Vol. 27
·期 10
·3127
·
IF 4.927
Miaomiao Chi,Kunming Qin,Lei Cao,Min Zhang,Yingying Su,Xun Gao
Coronary heart disease (CHD), which has developed into one of the major diseases, was reported to be treated by the target of peroxisome proliferators-activate receptor γ (PPAR-γ). As a natural medicine long used in the treatment of CHD, there are few studies on how to screen the target active compounds with high specific activity fromChoerospondias axillaris. To advance the pace of research on target-specific active compounds in natural medicines, we have combined magnetic ligand fishing and functionalized nano-microspheres to investigate the active ingredients of PPAR-γ targets inChoerospondias axillaris. The PPAR-γ functionalized magnetic nano-microspheres have been successfully synthesized and characterized by vibrating sample magnetometer (VSM), scanning electron microscopy (SEM), and transmission electron microscopy (TEM). The specificity, reusability, and reproducibility of the nano-microspheres were investigated with the help of the specific binding of rosiglitazone to PPAR-γ. In addition, the incubation temperature and the pH of the buffer solution in the magnetic ligand fishing were optimized to improve the specific adsorption efficiency of the analytes. Finally, with the aid of ultraperformance liquid chromatography plus Q-Exactive Orbitrap tandem mass spectrometry (UHPLC-Q-Exactive Orbitrap-MS/MS), the 16 active ligands including 9 organic acids, 5 flavonoids, and 2 phenols were found in the ethanolic extracts ofChoerospondias axillaris. Therefore, the study can provide a successful precedent for realizing the designated extraction and rapid isolation of target-specific active ingredient groups in the complex mixtures.Keywords:PPAR-γ;magnetic ligand fishing;Choerospondias axillaris;UHPLC-Q-Exactive orbitrap-MS/MS
研究领域:
药理学
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生物化学
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PubMed
高影响因子
International Journal of Nanomedicine
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2020
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IF 5.115
Shuping Wei,Chaoli Xu,Yidan Zhang,Zhongqing Shi,Min Wu,Bin Yang
Objective To investigate the antifibrotic effect of the combination of a PPARγ agonist-loaded nanoparticle-microbubble complex with ultrasound (US) exposure on renal interstitial fibrosis (RIF). Materials and Methods Polylactide-co-glycolide (PLGA) nanoparticles were used to load PPARγ agonist (rosiglitazone, RSG) and prepare PLGA-RSG nanoparticles (PLNPs-RSG); then, a novel complex between PLNPs-RSG and SonoVue microbubbles (MBs) (PLNPs-RSG-MBs) was prepared. The size distribution, zeta potentials, RSG-loading capacity and entrapment efficiency were measured, and the release of RSG was assessed using a UV-vis spectrophotometer. The in vitro cytotoxicity and in vivo systemic toxicity assays were performed. The cellular uptake assessment was performed using a confocal laser scanning microscope (CLSM). The in vivo biodistribution assessment was performed using fluorescence imaging with a near-infrared (NIR) imaging system. Furthermore, this complex was administered to a unilateral ureteral obstruction (UUO) rat model with the assistance of US exposure to investigate the antifibrotic effect. Results This PLNPs-RSG-MBs complex had a size of 2199.5± 988.1 nm and a drug-loading efficiency of 28.5%. In vitro cytotoxicity and in vivo systemic toxicity assays indicated that the PLNPs-RSG-MBs complex displayed excellent biocompatibility. In addition, the complex showed high cellular uptake efficiency in vitro and kidney-targeting ability in vivo. In a UUO rat model, the combination of the PLNPs-RSG-MBs complex with US exposure significantly reduced collagen deposition and successfully attenuated renal fibrosis. Conclusion The combination of the PLNPs-RSG-MBs complex with US exposure may be a promising approach for the treatment of RIF.
研究领域:
药理学
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纳米技术
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医学影像学
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肾脏疾病
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DOI
PubMed
高影响因子
INTERNATIONAL JOURNAL OF BIOLOGICAL MACROMOLECULES
·
2026
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IF 8.7
Yuanbiao Ma,Xu Liu,Zhewen Deng,Jiaqi Li,Ruoxi Liu,Shanshan Li,Can Zhang,Yutong Chen,Senqiang Zhu,Qi Zhang,Rui Liu,Bo Ma
CMCSMA/F127/TPGS@α-MG hydrogel promotes infected diabetic wound healing. • F127/TPGS micelles improve the aqueous solubility and sustained release of α-MG. • The composite hydrogel disrupts biofilms and achieves 99.6% wound closure. • α-MG modulates PPAR-γ, attenuating inflammation and promoting angiogenesis. Diabetic wounds pose a major clinical challenge owing to their complex microenvironment and persistent inflammation. To address this issue, we engineered a multifunctional, in situ photocrosslinkable composite hydrogel (CMCSMA/F127/TPGS@α-MG) to promote wound healing. To overcome the hydrophobicity of the antimicrobial agent α-mangostin (α-MG), it was first encapsulated in F127/TPGS nanomicelles. These micelles were then integrated into a methacrylated carboxymethyl chitosan (CMCSMA) matrix, enabling rapid conformal gelation upon 405 nm light irradiation. The resulting hydrogel exhibited a biphasic sustained-release profile, excellent biocompatibility, and potent contact-killing and anti-biofilm activities against Staphylococcus aureus ( S. aureus ). In an S. aureus -infected diabetic wound model, the hydrogel significantly accelerated wound closure, achieving 99.6% closure by day 14, and facilitated high-quality tissue regeneration characterized by complete re-epithelialization and orderly collagen deposition. Furthermore, an integrated approach combining network pharmacology, molecular docking, molecular dynamics simulations, and experimental validation revealed that the therapeutic efficacy of sustained local α-MG delivery involves the modulation of the PPAR-γ pathway. This regulatory process suppresses the NF-κB/COX-2 inflammatory axis and upregulates pro-angiogenic markers, including VEGF, CD31, and α-SMA. Collectively, this dual-action platform, which synergizes physical barrier protection with targeted molecular modulation, represents a promising translational strategy for refractory diabetic wounds. Schematic illustration of the preparation process and functional attributes of the in situ forming CMCSMA/F127/TPGS@α-MG hydrogel. Download: Download high-res image (67KB) Download: Download full-size image
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高影响因子
Stress Biology
·
2025
·Vol. 5
·期 1
·74
·
IF 5.8
Li Jie,Jiang Enhui,Zhang Mengyang,Pan Chuanying,Lei Chuzhao,Han Lin,Lan Xianyong
Ferroptosis has been increasingly implicated in adipose and muscle dysfunction, systemic metabolic disturbances, and several diseases in livestock, which necessitates effective and side-effect-free inhibition strategies. Phloretin, a dihydrochalcone with excellent antioxidant and anti-inflammatory properties, may have the potential to restrain cell ferroptosis. Herein, phloretin was verified to significantly inhibit (1S,3R)-RSL3-induced ferroptosis by reducing intracellular MDA, Fe 2 ⁺, and ROS levels and restoring cell total antioxidant capacity in bovine and mouse preadipocytes or myoblasts. It also alleviated oxidative stress (OS), a vital inducer of ferroptosis, by restoring antioxidant enzyme activity in the above cells and obese mice. In vivo, phloretin gavage significantly reversed the trend where high-fat diet (HFD)-induced OS promoted the expression of ferroptosis-promoting genes and proteins (e.g., ACSL4 and PTGS2) while inhibiting the expression of ferroptosis-negative regulators (e.g., Fth1 and Gpx4 ). Unlike most flavonoids that exert anti-inflammatory or antioxidant activities by altering the gut microbiota composition, metagenomic sequencing analysis of cecal contents from phloretin-gavaged and HFD mice revealed that phloretin exerts its antioxidative and ferroptosis-inhibitory effects independent of modulating gut microbiota diversity. Further transcriptomic analyses of mouse adipose tissues revealed that phloretin alleviated ferroptosis in adipocytes by modulating the transcription of genes enriched in AMPK and PPAR signaling pathways, such as Camkk2 . Hence, based on multi-omics analysis combined with in vivo and in vitro verification, phloretin effectively alleviated the OS to further inhibit ferroptosis of adipose or muscle cells through the AMPK-PPAR pathway, which can provide new research ideas for ameliorating adipose or myocyte dysfunction induced by ferroptosis in animals. Graphical
研究领域:
细胞生物学
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分子生物学
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动物科学
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营养学
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代谢紊乱
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氧化应激研究
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药理学
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DOI
PubMed
高影响因子
Drug Design Development and Therapy
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2023
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IF 4.8
Yi-Jin Wu,Sa-Sa Zhang,Qin Yin,Ming Lei,Qi-Hai Wang,Wen-Gang Chen,Ting-Ting Luo,Peng Zhou,Cong-Lan Ji
Background α-Mangostin (MG) showed the potentials in alleviating experimental arthritis, inhibiting inflammatory polarization of macrophages/monocytes, and regulating peroxisome proliferators-activated receptor γ (PPAR-γ) and silent information regulator 1 (SIRT1) signals. The aim of this study was to analyze the correlations among the above-mentioned properties.Methods Antigen-induced arthritis (AIA) was established in mouse, which was treated with MG in combination with SIRT1/PPAR-γ inhibitors to clarify the role of the two signals in the anti-arthritic actions. Pathological changes were systematically investigated. Phenotypes of cells were investigated by flow cytometry. Expression and co-localization of SIRT1 and PPAR-γ proteins in joint tissues were observed by the immunofluorescence method. Finally, clinical implications from the synchronous up-regulation of SIRT1 and PPAR-γ were validated by experiments in vitro.Results SIRT1 and PPAR-γ inhibitors (nicotinamide and T0070097) reduced the therapeutic effects of MG on AIA mice, and abrogated MG-induced up-regulation of SIRT1/PPAR-γ and inhibition of M1 polarization in macrophages/monocytes. MG has a good binding affinity to PPAR-γ, and MG promoted the co-expression of SIRT1 and PPAR-γ in joints. Synchronously activating SIRT1 and PPAR-γ was revealed to be necessary by MG to repress inflammatory responses in THP-1 monocytes.Conclusion MG binds PPAR-γ and excites this signaling to initiate ligand-dependent anti-inflammatory activity. Due to certain unspecified signal transduction crosstalk mechanism, it then promoted SIRT1 expression and further limited inflammatory polarization of macrophages/monocytes in AIA mice.
研究领域:
免疫学
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药理学
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风湿病学
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PubMed
高影响因子
Journal of Environmental Chemical Engineering
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2023
·
IF 7.7
Fei Shi,Minshan Yao,Yao Huang,Zhilong Chen,Jin Xiao,Fanbin Zhan,Yanan Li,Li Lin,Zhendong Qin
Antibiotics are used to treat illnesses in animals and humans worldwide. Yet, many antibiotics and other secondary metabolites can contaminate the water supply, creating a substantial risk to human health. A comprehensive investigation is currently focusing on the systematic effects of dietary antibiotics on fish liver, particularly on their impacts on oxidative stress , transcriptome profiles, toxicity, and apoptosis. In the present study, healthy grass carp were treated orally with 10 mg/kg enrofloxacin or florfenicol for 14 days. The enzyme activity outcomes reflected that the administration of enrofloxacin or florfenicol could significantly induce oxidative stress by decreasing CAT , SOD and GPx and increasing MDA. In addition, KEGG analysis showed that both antibiotics activated the PPAR signal pathway. The expression levels of the six genes, namely FABP6, APOA1, CYP27A1, ACSL1, CPT1A , and ANGPTL4, in the PPAR signal pathway were determined to further clarify the transcriptomic data. Enrofloxacin induced apoptosis in grass carp liver tissue, while hepatocytes from grass carp treated with enrofloxacin and florfenicol activated cytotoxicity and apoptosis. The present study suggests that antibiotics can induce antioxidant stress, impair the immune system, and attenuate the PPAR signal pathway in the grass carp liver, thus being harmful to grass carp as a dietary supplement, mainly within the aquaculture industry .
研究领域:
水产养殖
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毒理学
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分子生物学
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环境科学
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高影响因子
危险品化学品经营许可证（带存储）