ENVIRONMENTAL POLLUTION
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2026
·
IF 7.2
Yang Li,Yafang Yang,Xuan Li,Lu Qian,Chang Liu,Chenzhuo Nan,Yaxin Shen,Xinfeng Xing,Yuyan Xiong
Non-alcoholic fatty liver disease (NAFLD) is a prevalent metabolic disorder in which environmental exposures may play an important role. Dimethyl phosphate (DMP), a major dialkyl phosphate metabolite of organophosphorus pesticides, has traditionally been regarded primarily as a biomarker of exposure, whereas its potential biological role in NAFLD remains largely unexplored. In this study, we investigated whether DMP may exert biologically relevant effects in NAFLD progression and explored the underlying molecular mechanisms. Epidemiological analysis of 3050 participants from the National Health and Nutrition Examination Survey (NHANES) demonstrated a significant association between urinary DMP levels and NAFLD prevalence. Integrative bioinformatic analysis identified 24 DMP-NAFLD-related genes, among which six key NAFLD-associated genes were further prioritized, including four positively correlated genes (AURKA, CCNA2, WFDC2, and UBE2C) and two negatively correlated genes (NARS1 and SRSF3). These genes were subsequently incorporated into a diagnostic nomogram that exhibited good discriminative performance (AUC = 0.848). Connectivity mapping combined with exploratory molecular docking analyses further identified Pictilisib as a potential therapeutic candidate for DMP-induced NAFLD, with CCNA2 predicted to function as a key downstream target. In mice, DMP exposure induced hepatic steatosis, lipid accumulation, and metabolic dysfunction, which were partially attenuated by Pictilisib and genetic knockdown of CCNA2. Mechanistically, DMP increased CCNA2 expression and promoted a pro-inflammatory macrophage phenotype, as indicated by enhanced M1-like polarization and cytokine secretion. These effects were markedly attenuated by CCNA2 silencing, whereas re-expression of CCNA2 substantially restored the phenotype. In addition, conditioned medium from DMP-exposed macrophages induced lipid accumulation in hepatocytes through paracrine signaling. This effect was alleviated by CCNA2 silencing and restored by CCNA2 re-expression. These findings suggest that DMP may exert biological effects beyond its conventional role as an exposure biomarker and may contribute to NAFLD-related pathological processes, potentially through CCNA2-mediated macrophage-hepatocyte interactions.
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高影响因子
ENVIRONMENTAL RESEARCH
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2026
·
IF 8.2
Minming Chen,Yongjie Liu,Wenwen Qu,Qianlong Zhang,Fei Li,Yi Wang,Xuan Zhai
Per- and polyfluoroalkyl substances (PFASs) are persistent environmental contaminants closely linked to metabolic liver disease; however, the transgenerational hepatotoxicity and underlying mechanisms of emerging PFAS substitutes remain poorly understood. Herein, we focused on 6:2 polyfluoroalkyl phosphate diester (6:2 diPAP), a prominent PFAS substitute, to evaluate its developmental hepatotoxicity. By integrating zebrafish phenotyping, transcriptomic feature selection, virtual gene knockout, and experimental validation, we characterized the candidate molecular events through which 6:2 diPAP triggers non-alcoholic fatty liver disease (NAFLD)-like injury in offspring. Early-life exposure to environmentally relevant concentrations of 6:2 diPAP from 0 to 5 dpf, particularly 500 ng/L, induced persistent hepatic lipid accumulation, hepatic vacuolation, and metabolic disturbances in zebrafish at 28 dpf. Integrated network and transcriptomic analyses identified sequestosome 1 (SQSTM1) as a key stress-responsive hub associated with pathological hepatocyte remodeling. Quantitative real-time polymerase chain reaction (RT-qPCR) and immunofluorescence analyses further demonstrated exposure-responsive increases in sqstm1 expression and SQSTM1/p62 protein fluorescence intensity, with the strongest changes observed in the 500 ng/L group. Human single-nucleus RNA-seq and pseudotime analyses revealed that SQSTM1-high hepatocytes were enriched in injury-associated and senescence-associated states during NAFLD progression, suggesting a link between SQSTM1 activation and hepatocyte-state deterioration. Furthermore, virtual SQSTM1 knockout in NASH hepatocytes predicted oxidative stress, xenobiotic metabolic, and inflammatory rewiring. Molecular docking predicted a feasible 6:2 diPAP-SQSTM1 interaction with a binding affinity of −6.0 kcal/mol, and 200 ns molecular dynamics simulation supported the structural plausibility of the ligand-protein complex. Collectively, this study proposes a 6:2 diPAP-SQSTM1-hepatocyte remodeling axis and provides a comprehensive framework linking early-life PFAS exposure with hepatocyte-state transition and NAFLD-like metabolic dysfunction.
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高影响因子
JOURNAL OF AGRICULTURAL AND FOOD CHEMISTRY
·
2026
·
IF 6.7
Yinger Lan,Guanhong Jin,Xiaojuan Lei,Jichun Zhao,Lin Lei,Yalin Ran,Jian Ming
Abstract Nonalcoholic fatty liver disease (NAFLD) is characterized by excessive hepatic lipid accumulation, and the existing pharmacological alternatives are constrained by considerable side effects and probable toxicity. Orientin (Ori), a natural flavonoid with hepatoprotective potential, is restricted by poor solubility and low bioavailability. Herein, a galactosylated zein nanoplatform (Ori@Gal-Zein) was engineered via the Maillard reaction, resulting in uniform spherical nanoparticles (163.3 ± 2.6 nm) with high loading capacity of Ori (7.89 ± 0.14%) and gastrointestinal stability. In a CDAHFD-induced NAFLD mouse model, Ori@Gal-Zein decreased hepatic triglyceride and total cholesterol accumulation, attenuated lipid peroxidation, and restored antioxidant capacity, exhibiting comparable efficacy to silybin. Moreover, lipidomics revealed decreased triglyceride, diglyceride, and ceramide levels and restored the phosphatidylcholine/phosphatidylethanolamine ratio. Importantly, Ori@Gal-Zein remodeled gut microbiota by normalizing the Firmicutes/Bacteroidetes ratio, decreasing Pseudomonadota proliferation, and increasing Akkermansia abundance to alleviate NAFLD, providing a selection for carbohydrate-mediated protein nanoplatform.
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高影响因子
Journal of Functional Foods
·
2024
·
IF 3.8
Yunfei Wei,Meiyu Jin,Hao Yu,Xiaoning Hou,Lilei Zhao,Lu Ding,Jiaqi Cheng,Jiazhang Qiu,Haihua Feng
Glycyrrhiza glabra L. is a common heritage herbal medicine rich in antioxidant compounds such as flavonoids and triterpenoids. Non-alcoholic fatty liver disease has been the global prevalent chronic liver disorder. To investigate the curative role and mechanism of the Glycyrrhiza glabra L. crude extract on NAFLD, in vitro , we used oleic acid, palmitic acid, ML-385 and 3-MA to stimulate HepG2 cells. In vivo , we used Tyloxapol to inject mice intraperitoneally to establish an acute model, and high-fat diet to feed wild-type, Nrf2 -/- and ATG5 flox/flox mice to establish a chronic model. We used high performance liquid chromatography to analyse the content of major bioactive components in the Glycyrrhiza glabra L. crude extract. Our study found the Glycyrrhiza glabra L. crude extract could effectively alleviate lipid accumulation in non-alcoholic fatty liver disease, activate Nrf2 and promote autophagy. However, this alleviating effect disappeared when the Nrf2 and autophagy were inhibited separately. Our study demonstrates that crude extraction of active ingredients from traditional herbal medicines may be a potentially inexpensive, rapid and safe approach to alleviate lipid accumulation in non-alcoholic fatty liver disease.
研究领域:
药理学
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肝病学
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分子生物学
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高影响因子
BIOCHEMICAL PHARMACOLOGY
·
2026
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IF 6.5
Guowei Zhu,Junqing Yang,Dongzhi Ran,Ying Luo,Yanyi Wang,Wenjia Guo,Xiaodan Tan,Xiaobing Zhao,Yuanhong Gan,Huafeng Yin,Hong Wang
Non-alcoholic fatty liver disease (NAFLD) has become the fastest-growing etiology of cirrhosis and hepatocellular carcinoma. No Food and Drug Administration (FDA)-approved pharmacotherapy currently exists, underscoring the urgent need for novel regulatory circuits that can be translated into druggable targets. Here we demonstrate that autophagic flux is severely impaired and lipid accumulation markedly exacerbated in livers of NAFLD mouse models and in hepatocytes challenged with free fatty acid (FFA). Knock-down of metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) elevated miR-690 abundance, restored autophagic flux, and attenuated intracellular lipid deposition. Consistently, silencing methyltransferase-like 3 (METTL3) decreased MALAT1, thereby increasing miR-690 and producing the same protective phenotype, whereas METTL3 over-expression elicited the opposite effects. Mechanistically, METTL3 directly bound MALAT1 and installed N6-methyladenosine (m6A) modifications that enhanced MALAT1 stability and expression. Up-regulated MALAT1 subsequently sponged miR-690, leading to its functional depletion, autophagosome–lysosome fusion blockade, and aggravated lipid retention. Collectively, the METTL3-m6A/MALAT1/miR-690 axis orchestrates autophagy and lipid homeostasis, operationalizing an “m6A–long non-coding RNA (lncRNA)–microRNA (miRNA)” regulatory paradigm in NAFLD and offering an epitranscriptomic perspective on disease pathogenesis.
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高影响因子
Frontiers in Endocrinology
·
2026
·
IF 5.7
Yi Yao,Min Si,Hongcheng Ding,Chengcheng Cao,Hua Yang,Qianshu Sun
Background: Polycystic ovary syndrome (PCOS) and nonalcoholic fatty liver disease (NAFLD) are prevalent endocrine-metabolic disorders with a high comorbidity rate. However, their shared molecular mechanisms remain largely unclear. This study aimed to identify and validate key co-expressed genes driving PCOS-NAFLD comorbidity.Methods: Transcriptomic datasets for PCOS (GSE34526) and NAFLD (GSE89632) were analyzed using differential expression combined with three machine learning algorithms (LASSO, Random Forest, and XGBoost). Robustness was assessed using leave-one-out (LOO) resampling and nested cross-validation. Functional enrichment and PPI network analyses identified FCGBP as a key shared gene. A DHEA + high-fat diet–induced rat model was used to simulate key features of PCOS–NAFLD, and DHT+FFA-treated KGN and HepG2 cells were used for in vitro validation, with FCGBP silencing and rescue experiments performed to assess its functional role.Results: FCGBP expression was significantly elevated in both ovarian and hepatic tissues in the rat model (P < 0.01). In KGN cells, FCGBP knockdown restored E2 secretion and upregulated CYP19A1 and HSD17B1 (P < 0.001). In HepG2 cells, FCGBP silencing reduced lipid accumulation and reversed SCD1 upregulation and ATGL downregulation (P < 0.05). These effects were partially reversed by FCGBP re-expression (rescue), further supporting the specificity of its regulatory role. These findings indicate that FCGBP is associated with both hormonal dysregulation and hepatic lipid metabolic abnormalities under hyperandrogenic conditions.Conclusion: This study identifies FCGBP as a potential molecular regulator in PCOS–NAFLD comorbidity and a candidate target for modulating both reproductive and metabolic dysfunctions.
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高影响因子
Food & Function
·
2019
·Vol. 11
·期 1
·977-991
·
IF 3.241
Lihua Song,Yating li,Dan Qu,Pengling Ouyang,Xinwen Ding,PeiYing Wu,Qi Guan,Li Yang
Recent studies have shown that the occurrence and progression of nonalcoholic fatty liver disease (NAFLD) can be aggravated by dysregulation of intestinal flora. We previously found that phytosterol esters (PSEs) could effectively prevent the progression of NAFLD. Here, we further investigated the regulatory effect that PSEs have on gut flora and faecal metabolites in rats with NAFLD. Adult SD (Sprague Dawley) rats were randomized into four groups: the normal chow diet (NC), high-fat diet (HFD), low-dose PSE (0.05 g per 100 g BW, PSEL) and high-dose PSE (0.10 g per 100 g BW, PSEH) groups. PSEs were intragastrically administered once a day for 12 consecutive weeks. Our work indicated that high-dose PSE treatment effectively inhibited the increase in liver and abdominal fat indexes (P < 0.01) and hepatic lipids (P < 0.01); a high dose PSE treatment effectively corrected the HFD-induced intestinal flora imbalance by changing the diversity. The relative abundances of the four phyla (Firmicutes, Proteobacteria, Actinobacteria and Verrucomicrobia) and partial bacteria at the genus level (Faecalibacterium, Akkermansia, etc.) in the PSEH group were closer to those in the NC group. High-dose PSE intervention significantly increased the relative abundance of Bacteroidetes and Anaerostipes. Compared with the HFD, PSEH treatment significantly decreased the ionic strengths of bile acid metabolism products (P < 0.05), which were positively correlated with hepatic steatosis. In conclusion, PSE treatment exerts a beneficial effect on NAFLD that is associated with its regulatory action on intestinal flora and faecal metabolites, which might present a new opportunity to develop effective and safe preventive strategies against NAFLD.
研究领域:
营养学
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微生物学
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肝病学
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PubMed
高影响因子
INTERNATIONAL IMMUNOPHARMACOLOGY
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2023
·
IF 5.6
Sen Yang,Yang Zhang,Yan Zhang,Lianhong Yin,Xu Han,Xuerong Zhao,Ning Wang,Lina Xu
Long non-coding RNAs (lncRNAs) have been demonstrated to play vital roles in the pathogenesis of nonalcoholic fatty liver disease (NAFLD). However, their biological roles and function mechanisms in NAFLD remain largely unknown. In this study, we found that Gm28382 may be a potential pathogenic lncRNA of NAFLD and highly expressed in NAFLD through RNA-seq. Overexpression of Gm28382 significantly enhanced the lipid accumulation in AML12 cells, whereas Gm28382 silencing reduced lipogenesis both in palmitic acid (PA)-induced AML12 cells and high fat diet (HFD)-induced mice. Then, bioinformatics were employed to speculate the potential interacting genes of Gm28382, and found that Gm28382 may regulate ChREBP expression through binding with miR-326-3p. Fluorescence in situ hybridization (FISH), dual luciferase reporter assay, immunofluorescence RNA pull-down and RNA immunoprecipitation (RIP) assays were used to validate the binding and targeting relationship of these genes, and we confirmed that Gm28382 competitively binds to miR-326-3p to increase ChREBP expression as a ceRNA. Mechanistically, overexpression of Gm28382 upregulated the ChREBP-mediated lipid synthesis signaling pathway, but the function was sabotaged by miR-326-3p deletion or ChREBP overexpression. Furthermore, in PA-challenged AML12 cells or HFD-induced mice, silencing of Gm28382 reversed the aberrant ChREBP signaling pathway and lipid accumulation, whereas ChREBP overexpression or liver-specific silencing of miR-326-3p blocked this function of Gm28382. Collectively, these findings reveal a critical role of Gm28382 in the promotion of lipogenesis in NAFLD by regulating the ChREBP signaling pathway through interaction with miR-326-3p, which could serve as a potential therapeutic target for NAFLD treatment.
研究领域:
分子生物学
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生物化学
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肝病学
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基因组学
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病理学
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高影响因子
JOURNAL OF ETHNOPHARMACOLOGY
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2023
·
IF 5.4
Yating Guo,Qiushuang Sun,Shijiao Wang,Mengdi Zhang,Yuanyuan Lei,Jiejie Wu,Xinhong Wang,Wenjun Hu,Haitao Meng,Zhiyu Li,Luzhou Xu,Fang Huang,Zhixia Qiu
Ethnopharmacological relevance Along with the gradually increasing incidence, nonalcoholic fatty liver disease (NAFLD) has already been influencing the health of more and more people in the world. Corydalis saxicola Bunting (CSB), a valuable folk medicine, is the dried whole grass of a perennial herb, Yanhuanglian ( Papaveraceae ), which has significant effects on various hepatitis, liver fibrosis , cirrhosis and other liver diseases. Corydalis saxicola Bunting total alkaloids (CSBTA), a mixture of alkaloids extracted from CSB, exhibit widely-accepted hepatoprotective effects. Aim of the study This study aimed to explore the therapeutic potential of CSBTA on NAFLD and the underlying mechanism. Materials and methods A mice model was established by high fat and high cholesterol diet (HFHCD) to study the benefits of CSBTA on the progression of NAFLD. The efficacy of CSBTA on NAFLD was revealed systematically via RNA-sequencing analysis. Further efficacy and molecular mechanism study were explored in mouse primary hepatocytes and HepG2 cells stimulated with high energy with or without pharmacological inhibition or gene silencing. Results CSBTA effectively improved the major hallmarks of NAFLD including liver lipid accumulation, liver injury, inflammation and fibrosis in HFHCD-fed mice. RNA sequencing and targeted qPCR analysis jointly evidenced CSBTA significantly suppressed the expression of Srebf1 , Acc1 and Fasn which are the genes responsible for fatty acid biosynthesis. Moreover, stable isotope tracer test denoted CSBTA reduced lipid accumulation via interrupting fatty acid biosynthesis in hepatocytes or the liver. Mechanistically, CSBTA could impede SREBP1 maturation via AMPK activation, thereby reducing DNL-derived lipid accumulation in hepatocytes. Conclusions CSBTA protected against hepatic steatosis and other hallmarks of NAFLD induced by HFHCD via suppressing DNL, through modulating the AMPK-SREBP1 axis. CSBTA may therefore have a therapeutic potential for NAFLD treatment.
研究领域:
药理学
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肝病学
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分子生物学
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PubMed
高影响因子
PHYTOMEDICINE
·
2024
·
IF 6.7
Shanyi Yang,Zhijuan Wei,Jichu Luo,Xuancheng Wang,Guanghui Chen,Xuan Guan,Zhiyong She,Wenhui Liu,Ying Tong,Huan Liu,Mingsen Wen,Hongwei Chen,Pingchuan Zhu,Gui Li,Dongling Wang,Lin Huang,Siyi Xu,Danying Chen,Qisong Zhang,Ye Wei
Background Non-alcoholic fatty liver disease (NAFLD) poses a significant global public health concern. Liupao tea (LPT) is a Chinese national geographical indication product renowned for its lipid-lowering properties. However, the precise mechanisms and active constituents contributing to the efficacy of LPT against NAFLD remain unclear. Purpose This study aims to comprehensively explore the therapeutic potential of Liupao tea extract (LPTE) in alleviating NAFLD through an integrated strategy. Methods Initially, network pharmacology analysis was conducted based on LPTE chemical ingredient analysis, identifying core targets and key components. Potential active ingredients were validated through chemical standards based on LC-MS/MS. To confirm the pharmacological efficacy of LPTE in NAFLD, NAFLD mice models were employed. Alterations in hepatic lipid metabolism were comprehensively elucidated through integration of metabolomics, lipidomics, network pharmacology analysis, and real-time PCR analysis. To further explore the binding interactions between key components and core targets, molecular docking and microscale thermophoresis (MST) analysis were employed. Furthermore, to investigate LPTE administration effectiveness on gut microbiota in NAFLD mice, a comprehensive approach was employed. This included Metorigin analysis, 16S rRNA sequencing, molecular docking, and fecal microbiome transplantation (FMT). Results Study identified naringenin, quercetin, luteolin, and kaempferol as the potential active ingredients of LPTE. These compounds exhibited therapeutic potential for NAFLD by targeting key proteins such as PTGS2, CYP3A4, and ACHE, which are involved in the metabolic pathways of hepatic linoleic acid (LA) and glycerophospholipid (GP) metabolism. The therapeutic effectiveness of LPTE was observed to be comparable to that of simvastatin. Furthermore, LPTE exhibited notable efficacy in alleviating NAFLD by influencing alterations in gut microbiota composition ( Proteobacteria phylum, Lactobacillus and Dubosiella genus) that perhaps impact LA and GP metabolic pathways. Conclusion LPTE could be effective in preventing high-fat diet (HFD)-induced NAFLD by modulating hepatic lipid metabolism and gut microbiota. This study firstly integrated bioinformatics and multi-omics technologies to identify the potential active components and key microbiota associated with LPTE's effects, while also primally elucidating the action mechanisms of LPTE in alleviating NAFLD. The findings offer a conceptual basis for LPTE's potential transformation into an innovative pharmaceutical agent for NAFLD prevention.
研究领域:
药理学
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生物信息学
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代谢组学
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脂质组学
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胃肠病学
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微生物学
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PubMed
高影响因子
JOURNAL OF ETHNOPHARMACOLOGY
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2024
·
IF 4.8
Jin-Quan Zhao,Qi-Qi Zhou,Ke Liu,Ping Li,Yan Jiang,Hui-Jun Li
Ethnopharmacological relevance Celosia Semen (CS) serves as a traditional Chinese medicine (TCM) for promoting liver health and enhancing vision, with extensive clinical applications. Triterpenoid saponins represent the primary active components of CS, with the highest concentration of Celosin I (CI) detected. The urgent need for effective NAFLD treatments motivated us assess the beneficial effects of total saponins from CS (TSCS) and CI. Aims of the study To investigate the therapeutic effects of TSCS and CI on NAFLD and its underlying molecular mechanisms. Materials and methods The impact of TSCS and CI on NAFLD was evaluated through in vitro and in vivo methodologies, utilizing high-fat diet (HFD) and palmitic acid/oleic acid modeling on C57BL/6J mice and AML12 cells, respectively. Biochemical analysis, H&E and Oil red O staining were used to characterize the lipid-lowering and hepatoprotective activities of TSCS and CI. Lipidomics discerned the impact of TSCS and CI interventions on liver lipid composition, distribution and alteration in NFALD mice. RT-qPCR and western blotting detected the influence of TSCS and CI on genes linked to de novo lipogenesis, fat calculation uptake, oxidation and esterification. The docking analysis anticipated the interaction of six major triterpenoid saponins within TSCS with SREBP1. Results TSCS and CI markedly diminished lipid accumulation induced by high fat both in vivo and in vitro . TSCS and CI also mitigated hepatic steatosis and liver injury induced by HFD through the reduction of TC, TG, FAs, ALT, and AST, even at minimal dose of 25 mg/kg. Lipidomics indicated that TSCS and CI had the potential to modulate the lipid metabolism network, rectify lipid metabolic dysregulation induced by NAFLD, decrease the levels of harmful lipids, and elevate the levels of advantageous lipids. Furthermore, TSCS and CI exhibited a strong affinity to SREBP1, thereby might directly influence the expression of SREBP1 and a cascade of essential enzymes involved in de novo lipogenesis, and finally resulting in a diminished synthesis of novel lipids. Conclusion TSCS and CI were confirmed firstly as key active components of CS in amending hepatic steatosis and mitigate liver damage in NAFLD, outlining the preliminary mechanism. They warrant further exploration as drug candidates for NAFLD treatment, especially in light of the current shortage of medications and limited therapeutic options.
研究领域:
药理学
·
民族药理学
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脂质代谢
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分子生物学
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中药学
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PubMed
高影响因子
CARBOHYDRATE POLYMERS
·
2026
·
IF 13.2
Lu Zhang,Jiaxuan Li,Yue Hu,Haiyan Xiang,Xinpeng Cheng,Liqiang Zou,Yanru Zhou,Mingshun Chen
Urolithin A (UroA), a gut microbiota-derived metabolite of ellagitannins, has diverse biological activities but suffers from low water solubility and poor bioavailability. To address these challenges, this study developed gum arabic (GA)-coated UroA liposomes (UA-LPs-GA). The GA coating significantly enhanced the encapsulation efficiency, stability, and bioaccessibility of UroA. Pharmacokinetic studies showed that UA-LPs-GA improved the relative oral bioavailability of UroA by 3.09-fold compared to free UroA. In a high-fat diet-induced mouse model of non-alcoholic fatty liver disease (NAFLD), UA-LPs-GA administration effectively alleviated key pathological features, including hepatic steatosis, inflammation, and oxidative stress, with superior efficacy to free UroA. Mechanistic studies revealed that the hepatoprotective effects were mediated through activation of the AMPK/Nrf2 signaling pathway. Additionally, UA-LPs-GA positively modulated the intestinal flora, enriching beneficial bacteria and suppressing harmful taxa. This study establishes a practical approach to enhance UroA delivery and provides a new strategy for using functional polysaccharides in advanced delivery systems for NAFLD management.
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高影响因子
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