SURFACE & COATINGS TECHNOLOGY
·
2019
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IF 3.192
Baoqing Han,Guishan Wu,Hao Huang,Tinghan Liu,Jiuhong Wang,Jianhai Sun,Hairong Wang
The separation and detection of human breath play a significant role in early and non-invasive disease diagnosis. Various volatile organic compound (VOC) gases are considered as the biomarkers of a nonalcoholic fatty liver disease (NAFLD) patient. In this paper, a micro gas chromatography (GC) column used for VOCs separation of the NAFLD breath sample was presented, from its design, fabrication and separation performance testing. The serpentine column made using microelectromechanical system (MEMS) technology was chosen for its relatively small band broadening. The micro pillar configuration was simulated and optimized. The 3 m and 1 m long column with a cross-section of 200 μm × 240 μm was fabricated by deep-reactive-ion-etching (DRIE) method and sealed with anodic bonding. The stationary phase was coated to the inner wall of the column by static coating. The column was installed into the conventional gas chromatography to test separation performance of the GC. The nonpolar alkane mixture containing the NAFLD biomarker gas pentane was separated and the experimental factors such as the temperature and the carrier gas flow rate were studied. The results indicated that the micro GC column can effectively separate alkanes from C 5 -C 12 within 5 min. This could help the micro detector of micro GC system to quickly identify the contents or concentrations of characteristic alkanes. The micro GC column can meet the requirements of the micro GC system for the breath analysis of the NAFLD or other metabolic liver diseases. The micro column assembled with micro gas detector and preconcentrator can be hopefully developed into a portable breath analysis device.
研究领域:
分析化学
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医学诊断
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生物医学工程
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微流控
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DOI
高影响因子
Frontiers in Microbiology
·
2026
·
IF 5.8
Xiao-Long Wang,Chang Zhang,De-Shuang Lu,Zhuo-Yue Dong,Bai-Ming Jin,Si-Yuan Wan,Zi-Wen Zhang,Chun-Jing Zhang,Lin Li
Non-alcoholic fatty liver disease (NAFLD) is a widespread chronic metabolic disorder characterized by hepatic lipid accumulation, oxidative stress, inflammation and gut dysbiosis. Paeoniflorin (PAF) exhibits potential against NAFLD, yet its antioxidant mechanism via the gut-liver axis remains unclear. In a high-fat/sucrose (HFS) diet-induced NAFLD mouse model, C57BL/6 mice received PAF (50 or 100 mg/kg/day) for 10 weeks. Oxidative stress markers, histopathology, gut microbiota, and serum metabolomics were conducted, with fecal microbiota transplantation (FMT) applied for causal validation. PAF ameliorated metabolic disorders by suppressing hepatic lipogenesis and promoting cholesterol excretion. PAF significantly ameliorated oxidative stress by enhancing hepatic and colonic anti-oxidant capacity, evidenced by increased SOD activity and decreased MDA levels. It concurrently reduced systemic inflammation and enhanced intestinal barrier integrity via upregulation of tight junction proteins. Furthermore, PAF reshaped the gut microbiota, elevating beneficial Akkermansia and microbial-derived SCFAs, while suppressing pro-oxidant and pro-inflammatory pathogens like Desulfovibrio and Helicobacter. FMT confirmed that these antioxidant and metabolic benefits were mediated by the gut microbiota. In conclusion, PAF alleviates NAFLD primarily through potent antioxidant actions and anti-inflammatory, achieved via remodeling gut microbial ecology and reinforcing intestinal barrier.
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PubMed
高影响因子
INTERNATIONAL JOURNAL OF IMAGING SYSTEMS AND TECHNOLOGY
·
2024
·Vol. 34
·期 4
·e23123
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IF 3
Yuqiu Fu,Deyue Zang,Baiyou Lin,Qiming He,Yujie Xie,Baoliang Zhang,Yao Liu,Yi Jin,Yonghong He,Tian Guan
Nonalcoholic fatty liver disease (NAFLD) is a prevalent liver disorder affecting approximately 25.2% of the global population, posing risks of liver fibrosis, cancer, and metabolic disturbances. Despite its increasing prevalence, many facets of NAFLD's pathogenesis remain elusive, and there are currently no approved therapeutic drugs, underscoring the critical need for a comprehensive understanding of its pathophysiology to enable early diagnosis and intervention. Experimental animal studies play a pivotal role in elucidating the mechanisms underlying NAFLD and in the exploration of novel pharmacotherapies. Despite the widespread integration of deep learning techniques in human histopathology, their application to scrutinize histological features in animal models warrants exploration. This study presents a pioneering NAFLD assessment system leveraging IFNet and ResNet34 architectures. This automated system adeptly identifies inflammatory cell foci and hepatic steatosis in histopathology sections of rat livers. Remarkably, our approach achieved an impressive 95.6% accuracy in the assessment of hepatic steatosis and 77.7% in the evaluation of inflammation cell foci. By introducing a novel histopathology scoring system, our methodology mitigated subjective variations inherent in traditional pathologist evaluations, concurrently streamlining time and labor costs. This system ensured a standardized and precise assessment of rat liver histology in NAFLD and represented a significant stride toward enhancing the efficiency and objectivity of experimental outcomes.
研究领域:
病理学
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医学影像分析
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实验动物模型
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肝脏疾病研究
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DOI
高影响因子
CARBOHYDRATE POLYMERS
·
2022
·
IF 10.723
Pengchao Xie,Yan Peng,Liyan Qiu
To explore effective therapeutic strategy on nonalcoholic fatty liver disease (NAFLD), the amphiphilic oligochitosan derivative containing ursodeoxycholic acid (UDCA) was synthesized and named as UBC, which could self-assemble and encapsulate exenatide (Exe) to obtain Exe-UBC nano-vesicle. Exe-UBC could be uptaken by fatty-acid cultured cells and release UDCA and Exe responsive to the high esterase concentration. In vitro experiments demonstrated that Exe-UBC activated the expression level of SIRT1 with inhibited expression of PGC-1β and PPAR-γ and consequently exerted synergistic bioaction immediately on reducing lipidosis. After a month of Exe-UBC treated through intravenous injection, the body weight of high-fat diet feeding C57BL/6 mice recovered to ordinary level, and their lipid contents in the liver declined significantly. The recovery in hepatic function indexes like TG , AST , and ALT further revealed the superiority of Exe-UBC vesicles. These results suggested that the co-delivery of UDCA and Exe via Exe-UBC could be a potent platform for NAFLD treatment.
研究领域:
药学
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生物技术
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分子生物学
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药理学
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DOI
PubMed
高影响因子
JOURNAL OF NUTRITIONAL BIOCHEMISTRY
·
2023
·
IF 5.6
Peng Cao,Yi Wang,Cong Zhang,Mitchell A. Sullivan,Wen Chen,Xiang Jing,Huifan Yu,Fei Li,Qu Wang,Zhongshi Zhou,Qi Wang,Wen Tian,Zhenpeng Qiu,Lianxiang Luo
The global incidence of nonalcoholic fatty liver disease (NAFLD) has been surging in recent years, however, no drug is currently approved to treat this disease. Quercetin, a natural flavonoid abundant in plants and fruits, has been reported to alleviate NAFLD, however, the exact molecular mechanism remains unclear. This study aims to further elucidate its potential mechanism of action. The beneficial effects and the underlying mechanism of quercetin in alleviating NAFLD were explored both in vitro and in vivo, by employing chemical inhibitors of autophagosomes (3-methyladenine, 3-MA), autolysosomes (chloroquine, CQ), AMPK (Compound C, CC) and SIRT1 (selisistat, EX-527). The levels of intracellular lipids, reactive oxygen species, mitochondria function, autophagy, and mitophagy were assessed by fluorescent labeling and examined using flow cytometry or confocal microscopy. Key protein expressions of autophagy, mitophagy, and inflammation were also determined. In vivo, quercetin was shown to dose-dependently effectively alleviate NAFLD, but intraperitoneal injection of 3-MA could block the beneficial effects of quercetin on body weight, liver weight, serum ALT/AST, hepatic ROS and inflammation. In vitro, quercetin could reduce intracellular lipids (Nile Red staining) and ROS/DHE accumulation, which could be also blocked by 3-MA or CQ. Furthermore, we found that CC could abrogate the protective effects of quercetin on lipid and ROS accumulation in vitro. Also, CC abolished the proautophagic and anti-inflammatory effects of quercetin, as shown by western blot determination and Lyso-Tracker labeling. Importantly, mitophagy, a specific form of mitochondria-targeted autophagy, was enhanced by quercetin, as demonstrated by PINK1/Parkin protein variation and immunofluorescence colocalization of autophagosomes and mitochondria, which could also be blocked by the intervention of CC. This study demonstrates that quercetin prevents NAFLD through AMPK-mediated mitophagy and suggests that promoting mitophagy via an upregulation of AMPK may be a promising therapeutic strategy against NAFLD.
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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DOI
PubMed
高影响因子
PHYTOTHERAPY RESEARCH
·
2021
·Vol. 35
·期 7
·3898-3915
·
IF 5.882
Li Zhang,Sheng-Ye Yang,Feng-Rong Qi-Li,Xiao-Xiao Liu,Wei-Tao Zhang,Chao Peng,Ping Wu,Ping Li,Pingping Li,Xiaojun Xu
Isoliquiritigenin (ISO) is a flavonoid extracted from the root of licorice, which serves various biological and pharmacological functions including antiinflammatory, antioxidation, liver protection, and heart protection. However, the mechanism of its action remains elusive and the direct target proteins of ISO have not been identified so far. Through cell-based screening, we identified ISO as a potent lipid-lowering compound. ISO treatment successfully ameliorated fatty acid-induced cellular lipid accumulation and improved nonalcoholic fatty liver disease (NAFLD) and nonalcoholic steatohepatitis (NASH) by increasing PPARα-dependent lipid oxidation and decreasing SREBPs-dependent lipid synthesis. Both these signaling required the activation of SIRT1. Knockdown of SIRT1 resulted in the reversal of ISO beneficiary effects suggesting that the lipid-lowering activity of ISO was regulated by SIRT1 expression. To identify the direct target of ISO, limited proteolysis combined with mass spectrometry (LiP-SMap) strategy was applied and IQGAP2 was identified as the direct target for ISO in regulating lipid homeostasis. In the presence of ISO, both mRNA and protein levels of SIRT1 were increased; however, this effect was abolished by blocking IQGAP2 expression using siRNA. To explore how IQGAP2 regulated the expression level of SIRT1, proteome profiler human phospho-kinase array kit was used to reveal possible phosphorylated kinases and signaling nodes that ISO affected. We found that through phosphorylation of CREB, ISO transduced signals from IQGAP2 to upregulate SIRT1 expression. Thus, we not only demonstrated the molecular basis of ISO in regulating lipid metabolism but also exhibited for the first time a novel IQGAP2-CREB-SIRT1 axis in treating NAFLD/NASH.
研究领域:
药理学
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分子生物学
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肝病学
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DOI
PubMed
高影响因子
JOURNAL OF EXPERIMENTAL & CLINICAL CANCER RESEARCH
·
2025
·Vol. 44
·期 1
·330
·
IF 12.8
Liu Dan,Li Runtian,Li Mingzhu,Liang Ying,Wang Zhao,Sun Yang,Ge Pengling
Hepatocellular carcinoma (HCC), often arising from liver fibrosis in nonalcoholic fatty liver disease (NAFLD), remains a leading cause of cancer-related death. Targeting the gut–liver axis offers new therapeutic opportunities to prevent this progression. In this study, colon-targeted chitosan/pectin-based nanoparticles loaded with Astragalus polysaccharide (APs-CS/PT-NPs) were developed to modulate gut microbiota and inhibit liver tumorigenesis. The nanoparticles exhibited robust physicochemical stability and pH-responsive release. In vivo, oral administration of APs-CS/PT-NPs attenuated hepatic steatosis, reduced inflammatory cytokines, and suppressed NAFLD-induced HCC development. 16 S rRNA sequencing revealed restoration of microbial diversity and enhanced production of short-chain fatty acids, especially acetate. Mechanistically, transcriptomic profiling and functional analysis identified acetate as a key mediator, acting via G-protein-coupled receptor 43 (GPR43) to inhibit the NF-κB pathway. These results highlight the therapeutic potential of APs-CS/PT-NPs in modulating the gut–liver axis, rebalancing intestinal microbiota, and suppressing pro-inflammatory signaling. This nanoparticle-based strategy offers a promising food-derived preventive intervention for liver fibrosis–HCC transition. Graphical
研究领域:
药用纳米技术
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胃肠病学
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微生物组研究
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癌症预防
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免疫学
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天然产物药理学
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产品关联
DOI
PubMed
高影响因子
INTERNATIONAL JOURNAL OF MOLECULAR MEDICINE
·
2026
·Vol. 57
·期 4
·1-13
·
IF 8.5
Peng-Yao Lin,Jia-Rong Xie,Tian-Chen Qian,Shi-Song Wang,Si-Yi Yu,Wen-Bo Shi,Ying Wang,Lu-Ze Cen,Qing-Jing Zhu,Yi-Yang Zheng,Hui Gao,Rong Fang,Zhao-Xia Xia,Ai-Ming Liu,Lei Xu
International Journal of Molecular Medicine is an international journal devoted to molecular mechanisms of human disease.
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PubMed
高影响因子
CHEMICAL ENGINEERING JOURNAL
·
2026
·
IF 12.5
Kuiyou Wang,Xueqian Li,Kexin Huang,Deyuan Ning,Peishan Wang,Qiyan Lv,Hang Xu,Mingqian Tan,Yun Ma,Yujun Wan,Wentao Su
Ultrasound engineering increased probiotic EV yield while preserving immunoregulatory bioactivity. • Microfluidic loading enabled oral 300 W-EV@Fx with enhanced gastrointestinal stability and hepatic exposure. • 300 W-EV@Fx relieved hepatocyte lipotoxicity, oxidative injury, and metabolic dysfunction. • 300 W-EV@Fx improved hepatic macrophage balance and inflammatory homeostasis in HFD-fed mice. • EV depletion/add-back revealed hepatocyte EV–macrophage crosstalk in vitro . Nonalcoholic fatty liver disease (NAFLD) progression involves hepatocellular lipotoxicity together with amplification of the hepatic inflammatory microenvironment. Therapeutic strategies that simultaneously alleviate hepatocyte injury and hepatic immune dysregulation remain underexplored. Here, we generated acoustically augmented probiotic extracellular vesicles from Lacticaseibacillus casei . Among them, vesicles generated under 300 W ultrasound stimulation (300 W-EV) showed an optimal balance of enhanced yield, structural integrity, and immunomodulatory activity. Fucoxanthin (Fx) was then encapsulated using microfluidic technology to construct an oral nanodelivery platform, 300 W-EV@Fx. In vivo , orally administered 300 W-EV@Fx showed enhanced hepatic exposure within 8 h, alleviated hepatic lipid deposition and oxidative damage in high-fat diet-fed mice, restored mitochondrial respiration, and ameliorated immune dysregulation characterized by Treg loss, macrophage infiltration, and M1-like/M2-like imbalance. In complementary mechanistic studies performed in vitro , 300 W-EV@Fx relieved lipotoxic hepatocyte injury. Coculture and EV depletion/add-back experiments further showed that hepatocyte-derived EVs functionally contributed to macrophage inflammatory responses. EVs from lipotoxic hepatocytes promoted macrophage ROS accumulation, inflammatory polarization, and glycolytic activation, whereas EVs from 300 W-EV@Fx-treated hepatocytes drove macrophage immunometabolic reprogramming toward an anti-inflammatory phenotype supported by mitochondrial oxidative metabolism. Overall, this study presents an oral delivery strategy that integrates efficient drug delivery with microenvironmental regulation, attenuating NAFLD progression through the coordinated relief of hepatocellular lipotoxicity and inflammatory microenvironmental imbalance.
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DOI
高影响因子
International Journal of Nanomedicine
·
2024
·
IF 6.6
Jianmei Lu,Yongzhu Zeng,Huashuai Zhong,Wei Guo,Yuyan Zhang,Wanting Mai,Yucui Qin,Xiaodan Su,Bo Zhang,Weisen Wu,Yu Zhu,Qiujie Huang,Yong Ye
Background and Purpose Nitidine chloride (NC) is a botanical drug renowned for its potent anti-inflammatory, antimalarial, and hepatocellular carcinoma-inhibiting properties; however, its limited solubility poses challenges to its development and application. To address this issue, we have devised a colon-targeted delivery system (NC-CS/PT-NPs) aimed at modulating the dysbiosis of the gut microbiota by augmenting the interaction between NC and the intestinal microbiota, thereby exerting an effect against nonalcoholic fatty liver disease.Methods The NC-CS/PT-NPs were synthesized using the ion gel method. Subsequently, the particle size distribution, morphology, drug loading efficiency, and release behavior of the NC-CS/PT-NPs were characterized. Furthermore, the impact of NC-CS/PT-NPs on non-alcoholic fatty liver disease (NAFLD) induced by a high-fat diet (HFD) in mice was investigated through serum biochemical analysis, ELISA, and histochemical staining. Additionally, the influence of NC-CS/PT-NPs on intestinal microbiota was analyzed using 16S rDNA gene sequencing.Results The nanoparticles prepared in this study have an average particle size of (255.9±5.10) nm, with an encapsulation rate of (72.83±2.13) % and a drug loading of (4.65±0.44) %. In vitro release experiments demonstrated that the cumulative release rate in the stomach and small intestine was lower than 22.0%, while it reached 66.75% in the colon. In vivo experiments conducted on HFD-induced NAFLD mice showed that treatment with NC-CS/PT-NPs inhibited weight gain, decreased serum aspartate aminotransferase (AST), Alanine aminotransferase (ALT) and lipid levels, improved liver and intestinal inflammation, and altered the diversity of gut microbiota in mice.Conclusion This study provides new evidence for the treatment of NAFLD through the regulation of gut microbiota using active ingredients from traditional Chinese medicine.
研究领域:
药学
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生物技术
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胃肠病学
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代谢学
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产品关联
DOI
PubMed
高影响因子
Food Bioscience
·
2023
·
IF 5.2
Wenya Ke,Juan Huang,Yi Zhong,Yuhong Shi,Fen Yan,Da Huang,Yuanzi Wu,Houbing Zheng,Zuquan Weng
Non-alcoholic fatty liver disease (NAFLD) has become a globally rising issue that can cause liver-related morbidity and mortality. Recent studies have revealed that a high-fat diet (HFD) highly contributes to the prevalence and progression of NAFLD via impacting gut microbiota and lipid metabolism signal pathways. Resveratrol (RSV), a natural bioactive compound , has exhibited potential for preventing and alleviating NAFLD. However, due to the poor bioavailability of RSV, its strengths and underlying mechanisms for NAFLD therapeutic potential are poorly understood. To address this, we utilized Hydroxypropyl-beta-Cyclodextrin (HBC) to encapsulate RSV to enhance its water solubility and conducted prevention and intervention experiments in HFD-fed mice. The results showed that the HBC has significantly enhanced the water solubility of RSV by 250-fold and the HBC-RSV better prevented and alleviated the liver steatosis, obesity and abnormal lipid metabolism induced by HFD than RSV alone. Meanwhile, combining HFD and HBC-RSV or RSV prevented HFD mice progressing to NAFLD. Besides, further investigation indicated that RSV could resist liver injury and obesity by modulating gut microbiota, raising the levels of short-chain fatty acids (SCFAs) and activating AMP-activated protein kinase (AMPK) signaling pathway . The activated pathway down-regulated sterol receptor element binding protein 1c (SREBP1c) and acetyl-coenzyme A carboxylase (ACC) to decrease lipid synthesis and up-regulated peroxisome proliferators-activated receptorα (PPARα) to promote the fatty acid oxidation , thus preventing NAFLD. Our findings suggested that water solubility-enhanced RSV beneficially modulated gut microbiota, altered gut microbiota-derived SCFAs, and activated lipid metabolism regulatory pathways, providing potential for NAFLD prevention and alleviation.
研究领域:
药理学
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肝病学
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微生物组研究
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代谢性疾病
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DOI
高影响因子
Frontiers in Endocrinology
·
2023
·
IF 5.2
Tingwan Du,Lian Xiang,Jingjing Zhang,Chunmei Yang,Wenxin Zhao,Jialu Li,Yong Zhou,Ling Ma
Introduction The study aimed to explore the association of serum 25(OH)D 3 and hepatic steatosis in non-alcoholic fatty liver disease (NAFLD) patients and to determine whether the effect of vitamin D (VD) is mediated by activation of the peroxisome proliferator-activated receptor α (PPARα) pathway. Methods The study contained a case-control study, in vivo and in vitro experiments. A case-control study was conducted to compare serum parameters between NAFLD patients and controls and to evaluate the association of 25(OH)D 3 and NAFLD. In vivo study, male Wistar rats were randomly divided into control and model groups, fed a standard chow diet and a high-fat diet (HFD), respectively, for 7 weeks to generate an NAFLD model. Then, the rats were treated with VD and a PPARα antagonist (MK886) for 7 weeks. Tissue and serum were collected and assessed by biochemical assays, morphological analysis, histological analysis, and western blot analysis. In vitro , HepG2 cells were incubated with oleic acid (OA) to induce steatosis, which was evaluated by staining. HepG2 cells were pretreated with MK886 followed by calcitriol treatment, and differences in lipid metabolism-related proteins were detected by western blot. Results NAFLD patients were characterized by impaired liver function, dyslipidemia, and insulin resistance. Serum 25(OH)D 3 was negatively associated with alanine aminotransferase (ALT) in NAFLD. VD deficiency was a risk factor for patients with no advanced fibrosis. Adequate VD status (25(OH)D 3 >20 ng/mL) had a protective effect in patients after adjustment for confounding variables. NAFLD rats showed hyperlipidemia with severe hepatic steatosis, systematic inflammation, and lower serum 25(OH)D 3 . VD treatment ameliorated hepatic steatosis both in NAFLD rats and OA-induced HepG2 cells. Further, MK886 inhibited the anti-steatosis effect of VD. Conclusion The study revealed that an adequate VD level may act as a protective factor in NAFLD and that VD may alleviate hepatic steatosis via the PPARα signaling pathway.
研究领域:
肝病学
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内分泌学
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营养学
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分子生物学
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产品关联
DOI
PubMed
高影响因子
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