Journal of Analytical Methods in Chemistry
·
2025
·Vol. 2025
·期 1
·4646858
·
IF 2.2
Gui-Yu Li,Bai-Xue Li,Hong-Fei Song,Jie-Wen Gou,Li Wen,Quan-Sheng Feng
Background and Objectives: Liver fibrosis results from chronic inflammation. Qijia Rougan decoction, a traditional Chinese medicinal formulation, shows hepatoprotective potential, yet its mechanisms remain unclear. This study aims to investigate its antifibrotic effects and underlying mechanisms. Methods: Rat liver fibrosis was induced by carbon tetrachloride (CCl 4 ) and ethanol exposure. Histopathological assessment was performed using hematoxylin–eosin (HE) and Masson’s trichrome staining. Hepatic stellate cell (HSC) activation and autophagic processes were examined through western blot analysis, immunofluorescence staining, and other in vitro assays. Components of Qijia Rougan decoction were analyzed by BATMAN-TCM platform. The pharmacological network was constructed using BATMAN-TCM platform, while disease-related targets were identified through DisGeNET database. Pathway enrichment analysis was conducted using KEGG pathway database. Results: Significant reductions in hepatic index and serum biomarkers (ALT, AST, ALP, TBA, and γ-GT) were observed following Qijia Rougan decoction treatment, with maximal efficacy at 6 weeks. The decoction downregulated of LC3B and α-SMA expression in fibrotic tissues. In vitro, it suppressed LPS-induced α-SMA expression and autophagosome formation in HSC-T6 cells. Network pharmacology analysis of Qijia Rougan decoction identified 274 bioactive compounds and 12,883 potential targets, with pathway analysis indicating PI3K/AKT signaling as the predominant regulatory mechanism. Conclusion: Qijia Rougan decoction alleviates liver fibrosis, potentially by inhibiting HSC activation and autophagy processes via PI3K/AKT/mTOR pathway.
研究领域:
药理学
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肝脏病学
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DOI
PubMed
高影响因子
JOURNAL OF MEDICAL VIROLOGY
·
2025
·Vol. 97
·期 5
·e70395
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IF 4.6
Qiuhong You,Kaifeng Wang,Zhou Zhao,Heqi Zhou,Zhixian Lan,Hongyan Liang,Rui Deng,Wanying Li,Sheng Shen,Routing Wang,Kaikai Zhang,Dekai Zheng,Jian Sun
In chronic hepatitis B (CHB) patients under antiviral treatment, liver injury, as evidenced by elevated alanine transaminase (ALT), is associated with unfavorable outcomes and needs effective treatment. The interaction between gut microbiota and liver injury in CHB patients remains unclear. Using a case-control design, 28 cases with elevated ALT and 28 matched controls with normal ALT were randomly selected from CHB patients with viral control. Clinical characteristics were comparable between groups. Metagenomic sequencing revealed that Bacteroides fragilis was decreased in cases and exhibited the greatest disparity between cases and controls. Mice colonized by gut microbiota from cases exhibited more severe liver damage in both LPS-induced and MCD diet-induced liver injury models, and had a lower abundance of B. fragilis compared to mice colonized by gut microbiota from controls. Oral gavage of B. fragilis improved both LPS-induced and MCD diet-induced liver injury. Metabolomics analysis revealed that the levels of 7-Ketolithocholic acid (7-Keto-LCA) were positively correlated with B. fragilis and significantly increased in the cultural supernatant of B. fragilis . Consistently, 7-Keto-LCA exerted protective effects against both LPS-induced and MCD diet-induced liver damage. Targeting gut microbiota might be a promising therapeutic treatment for alleviation residual liver inflammation in CHB patients with viral control.
研究领域:
医学
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微生物学
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代谢组学
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DOI
PubMed
高影响因子
INTERNATIONAL JOURNAL OF BIOLOGICAL MACROMOLECULES
·
2019
·
IF 4.784
Rui Jiang,Song Zhao,Langkun Chen,Maoyu Zhao,Wenjing Qi,Wensheng Fu,Lianzhe Hu,Yan Zhang
In this research, a new DSA (Distyryl-anthracene) derivative with four carboxyl groups was designed and synthesized. This molecule exhibits aggregation-induced emission property (AIE). With the AIE character, a convenient and sensitive fluorescent probe for the detection of protamine , heparin and heparinase has been developed. The protamine can directly induce the aggregation of probe, which caused by electrostatic attraction. In this way, the turn-on detection of protamine is achieved, and the detection limit is as low as 30 ng mL −1 . When heparin appears, the probes will be redisperse in solution, which causes a decrease in fluorescence intensity. Besides, this method also shows good selectivity and sensitivity, and the linear range of heparin is from 0.08 to 8 μg mL −1 with detection limit of 37 ng mL −1 . After hydrolyzing heparin by heparinase, the probes rebind with protamine and the fluorescence enhance. The fluorescence enhancement was linearly related to the concentration of heparinase in the range of 0.02–2.0 μg mL −1 and detection limit as low as 143.7 ng mL −1 . In addition, the results exhibited that the recovery percentage of heparinase in bovine samples reached to 96–101%.
研究领域:
生物化学
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分析化学
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DOI
高影响因子
JOURNAL OF ANIMAL SCIENCE
·
2024
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IF 2.7
Liu Jie,Zhang Ke,Zhao Mindie,Chen Liang,Chen Huimin,Zhao Yulan,Zhao Ruqian
The aim of this study was to investigate the alleviating effects and mechanisms of bile acids (BA) on corticosterone-induced fatty liver in broiler chickens. Male Arbor Acres chickens were randomly divided into three groups: control group (CON), stress model group (CORT), and BA-treated group (CORT-BA). The CORT-BA group received a diet with 250 mg/kg BA from 21 days of age. From day 36 to 43, both the CORT and CORT-BA groups received subcutaneous injections of corticosterone to simulate chronic stress. The results indicated that BA significantly mitigated the body weight loss, liver enlargement, and hepatic lipid deposition caused by corticosterone (P < 0.05). Liver RNA-seq analysis showed that BA alleviated corticosterone-induced fatty liver by inhibiting lipid metabolism pathways, including fatty acid biosynthesis, triglyceride biosynthesis, and fatty acid transport. Additionally, BA improved corticosterone-induced downregulation of glucocorticoid receptor (GR) expression (P < 0.05). Molecular docking and cellular thermal shift assays revealed that hyodeoxycholic acid (HDCA), a major component of compound bile acids, could bind to GR and enhance its stability. In conclusion, BA alleviated corticosterone-induced fatty liver in broilers by inhibiting lipid synthesis pathways and mitigating the suppression of hepatic GR expression.
研究领域:
动物科学
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分子生物学
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营养学
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DOI
PubMed
高影响因子
JOURNAL OF NANOBIOTECHNOLOGY
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2020
·Vol. 18
·期 1
·1-11
·
IF 6.518
Ji De,Wang Qiaohan,Zhao Qi,Tong Huangjin,Yu Mengting,Wang Meng,Lu Tulin,Jiang Chengxi
Hepatic stellate cells (HSCs) were activated and secreted excessive amounts of extracellular matrix (ECM) proteins during pathogenetic progress of liver fibrosis. Germacrone (GMO) and miR-29b can play an important role in inhibiting growth of HSCs and production of type I collagen. GMO and miR-29b were co-encapsulated into nanoparticles (NPs) based on poly(ethylene glycol)-block-poly(lactide-co-glycolide) (PEG-PLGA). Then, NPs were modified with cyclic RGD peptides (cRGDfK). cRGDfK is an effective ligand to bind integrin αvβ3 and increase the targeting ability for fibrotic liver. GMO- and miR-29b-loaded NPs exhibited great cytotoxicity to activated HSCs and significantly inhibited production of type I collagen. Liver fibrosis model of mice was induced by administration of carbon tetrachloride. Great targeting ability was achieved in liver fibrotic mice treated with cRGD-modified NPs. Significant ant-fibrotic effects have been presented based on hematoxylin and eosin (H&E), Masson and Sirius Red staining results of liver tissues collected from mice treated with drug-loaded NPs. All these results indicate GMO- and miR-29b-loaded cRGD-modified NPs have the potential for clinical use to treat liver fibrosis.
研究领域:
药理学
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分子生物学
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纳米医学
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DOI
PubMed
高影响因子
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
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2022
·Vol. 23
·期 15
·8081
·
IF 6.208
Xueqin Wang,Huahua Yu,Ronge Xing,Pengcheng Li
Alcohol-induced liver disease (ALD) has become one of the major global health problems, and the aim of this study was to investigate the characterization of the structure as well as the hepatoprotective effect and mechanism of oyster peptide (OP, MW < 3500 Da) on ALD in a mouse model. The results demonstrate that ethanol administration could increase the activities of aspartate aminotransferase (AST), alanine transaminase (ALT), γ-Glutamyl transferase (GGT), reactive oxygen species (ROS), malondialdehyde (MDA), and triglycerides (TG), as well as increase the interleukin-1β (IL-1β), interleukin-6 (IL-6), and tumor necrosis factor (TNF-α) levels (p< 0.01), and reduce the activity of superoxide dismutase (SOD) and the concentration of glutathione (GSH). Those changes were significantly reversed by the application of different doses of OP. Furthermore, the mRNA expressions of nuclear factor elythroid 2-related factor 2 (Nrf2), heme oxygenase-1 (HO-1), and quinone oxidoreductase1 (NQO1) were significantly up-regulated in OP groups, and the mRNA expressions of nuclear factor kappa-light chain enhancer of B cells (NF-κB), TNF-α, and IL-6 were markedly reduced in OP groups compared to that of the model group. Thus, OP had a significant protective effect on ALD through the enhancement of the in vivo antioxidant ability and the inhibition of the inflammatory response as possible mechanisms of action, which therefore suggests that OP might be useful as a natural source to protect the liver from alcohol damage.Keywords:oyster peptide;alcohol-induced liver diseases;hepatoprotective effect;oxidative stress;inflammatory response
研究领域:
肝脏病学
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营养保健品
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分子生物学
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DOI
PubMed
高影响因子
RSC Advances
·
2017
·Vol. 7
·期 14
·8178-8185
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IF 3.108
Xueyang Fang,Xianlin Wu,Chang'e Li,Binwei Zhou,Xiaoyin Chen,Tianfeng Chen,Fang Yang
As a traditional Chinese medicine, baicalin exhibits high antitumor activity towards hepatitis B virus (HBV)-infected liver cancer, but low toxicity towards normal tissues. However, the properties of baicalin, including its low hydrophilicity and poor biocompatibility, have limited its clinical application. Herein, in this study, we have designed and synthesized multifunctional selenium nanoparticles (SeNPs) with baicalin (B) and folic acid (FA) surface-modifications for the targeted treatment of HBV infected liver cancer. B–SeNPs–FA showed appropriate particle size distribution, high stability, and higher cellular uptake by tumor cells than normal cells. The nanoparticles primarily targeted lysosomes in HepG2215 cells through utilization of the main pathways of caveolae-mediated endocytosis and energy-dependent endocytosis. B–SeNPs–FA induced HepG2215 cell apoptosis by down-regulating the generation of reactive oxygen species (ROS) and the expression of the HBxAg protein. In addition, B–SeNPs–FA exhibited an excellent ability to inhibit cancer cell migration and invasion. Taken together, these results suggest that baicalin-loaded selenium nanoparticles with a folic acid targeting moiety could be a promising strategy for the design and synthesis of cancer-targeted nanomaterials to treat HBV-infected liver cancer.
研究领域:
药理学
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肿瘤学
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纳米医学
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产品关联
DOI
高影响因子
PHYTOMEDICINE
·
2023
·
IF 7.9
Yong Fang Gong,Shu Hou,Jia-Cheng Xu,Yan Chen,Le-Le Zhu,Ying-Ying Xu,Yu-Qing Chen,Miao-Miao Li,Li-Li Li,Jing-Jing Yang,Yan Yang
Background Phosphorylated Smad3 isoforms are reversible and antagonistic, and the tumour-suppressive pSmad3C can shift to an oncogenic pSmad3L signal. In addition, Nrf2 has a two-way regulatory effect on tumours, protecting normal cells from carcinogens and promoting tumour cell survival in chemotherapeutics. Accordingly, we hypothesised that the transformation of pSmad3C/3L is the basis for Nrf2 to produce both pro- and/or anti-tumourigenic effects in hepatocarcinogenesis . Astragaloside IV (AS-IV), the major component of Astragalus membranaceus , exerts anti-fibrogenic and carcinogenic actions. Lately, AS-IV administration could delay the occurrence of primary liver cancer by persistently inhibiting the fibrogenesis and regulating pSmad3C/3 L and Nrf2/HO-1 pathways synchronously. However, effect of AS-IV on hepatocarcinogenesis implicated in the bidirectional cross-talking of pSmad3C/3 L and Nrf2/HO-1 signalling, especially which one contributes palpably than the other still remains unclear. Purpose This study aims to settle the above questions by using in vivo (pSmad3C +/− and Nrf2 −/− mice) and in vitro (plasmid- or lentivirus- transfected HepG2 cells) models of HCC . Study design and methods The correlation of Nrf2 to pSmad3C/pSmad3L in HepG2 cells was analysed by Co-immunoprecipitation and dual-luciferase reporter assay. Pathological changes of Nrf2, pSmad3C, and pSmad3L in human HCC patients, pSmad3C +/- mice, and Nrf2 −/- mice were gauged by immunohistochemical, haematoxylin and eosin staining, Masson, and immunofluorescence assays. Finally, western blot and qPCR were used to verify the bidirectional cross-talking of pSmad3C/3L and Nrf2/HO-1 signalling protein and mRNA in vivo and in vitro models of HCC. Results Histopathological manifestations and biochemical indicators revealed that pSmad3C +/- could abate the ameliorative effects of AS-IV on fibrogenic/carcinogenic mice with Nrf2/HO-1 deactivation and pSmad3C/p21 transform to pSmad3L/PAI-1//c-Myc. As expected, cell experiments confirmed that upregulating pSmad3C boosts the inhibitory activity of AS-IV on phenotypes (cell proliferation, migration and invasion), followed by a shift of pSmad3L to pSmad3C and activation of Nrf2/HO-1. Synchronously, experiments in Nrf2 −/- mice and lentivirus-carried Nrf2shRNA cell echoed the results of pSmad3C knockdown. Complementarily, Nrf2 overexpression resulted in the opposite result. Furthermore, Nrf2/HO-1 contributes to AS-IV's anti-HCC effect palpably compared with pSmad3C/3L. Conclusion These studies highlight that harnessing the bidirectional crosstalk pSmad3C/3 L and Nrf2/HO-1, especially Nrf2/HO-1 signalling, acts more effectively in AS-IV's anti-hepatocarcinogenesis, which may provide an important theoretical foundation for the use of AS-IV against HCC.
研究领域:
分子生物学
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癌症研究
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药理学
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细胞生物学
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产品关联
DOI
PubMed
高影响因子
Frontiers in Pharmacology
·
2025
·
IF 4.8
Yan Liu,Feng Qi,Lun-Jian Xiang,Zhu-Jun Yi,Sheng-Wei Li
Background: Donation after circulatory death (DCD) livers are limited by mandatory warm ischemia and are more susceptible to ischemia‒reperfusion injury (IRI). Inflammation and oxidative stress play key roles in the development of hepatic IRI, and Rutaecarpine (Rut) has anti-inflammatory and anti-oxidative stress effects. The aim of this study was to investigate whether Rut can alleviate hepatic IRI in liver transplantation (LT) and to explore the underlying mechanisms.Methods: Rat DCD LT and oxygen-glucose deprivation/reoxygenation (OGD/R) cell models were established to clarify the effect of Rut on hepatic IRI. The key molecules involved in the hepatoprotective effects of Rut were identified through joint analysis of data from LT patients and drug targets. The target was further validated by in silico, in vivo and in vitro experiments.Results: Rut significantly alleviated liver dysfunction, pathological injury, and apoptosis and improved the survival rate of the rats subjected to LT. In addition, Rut significantly inhibited inflammatory response and oxidative stress. Rut also had similar effects on OGD/R-induced hepatocyte injury. Mechanistically, bioinformatics analysis and in vivo and in vitro experiments revealed that PDE4B may be a key target by which Rut exerts its protective effect, and molecular docking and cellular thermal shift assay confirmed this result. The function of PDE4B was studied via gene intervention technology, and the results showed that PDE4B can aggravate hepatic IRI. Furthermore, PDE4B overexpression abrogated the protective effect of Rut on the liver in LT.Conclusion: Rut alleviates hepatic IRI by targeting PDE4B to inhibit inflammation and oxidative stress. These findings highlight the potential of Rut as a drug candidate for the treatment of patients undergoing LT.
研究领域:
药理学
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移植学
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肝病学
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分子生物学
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产品关联
DOI
PubMed
高影响因子
Food & Function
·
2020
·Vol. 11
·期 5
·4582-4590
·
IF 4.171
Xiaohua Lei,Qiang Liu,Qiang Liu,Zhenyu Cao,Ju Zhang,Tao Kuang,Yu Fang,Guoxing Liu,Ke Qian,Jie Fu,Huihui Du,Zhiqiang Liu,Zhihong Xiao,Changzhu Li,Xundi Xu
Liver fibrosis is a common part of the pathological development of many chronic liver diseases. As liver fibrosis progresses, it may lead to cirrhosis, portal hypertension, liver decompensation, liver tumours, and death. Camellia oil (Camellia oleifera Abel.) is widely used as an edible oil in China. It has a wide range of biological activities and is used as a traditional medicine to treat conditions such as burns and stomach pains. However, whether camellia oil can ameliorate liver fibrosis remains unclear. We constructed a liver fibrosis model induced by carbon tetrachloride (CCl4) and then confirmed the role of camellia oil in liver fibrosis by biochemical examination, histopathological morphology, immunohistochemistry, and western blot analysis. We found that camellia oil ameliorated histopathological lesions, improved liver function and antioxidant capacity, decreased the expression of TGF-β1 and α-SMA proteins, and downregulated the expression of the pro-apoptotic proteins in CCl4-induced liver fibrosis. Therefore, these results suggest that camellia oil attenuates CCl4-induced liver fibrosis in mice, and its mechanism may function via reduction of hepatocyte apoptosis to inhibit hepatic stellate cell (HSC) activation. Camellia oil may provide a potential new treatment for liver fibrosis as an auxiliary treatment by addition of the edible oil to the daily diet.
研究领域:
药理学
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肝病学
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病理学
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产品关联
DOI
PubMed
高影响因子
ENVIRONMENTAL POLLUTION
·
2022
·
IF 9.988
Zhiying Miao,Zhiruo Miao,Xiaohua Teng,Shiwen Xu
As a widespread aquatic environmental contaminant, Lead (Pb) can provoke hepatic injury in various animals. Melatonin (MT) plays a crucial role in the regulation of inflammatory response. Accumulating evidence elucidates exogenous toxins can elicit hepatic lipid metabolic disorders by influencing the gut microbiome. Nevertheless, the effects of Pb on gut microbiota and hepatic lipid metabolism of the common carps, and whether MT can prevent and cure Pb-induced toxicity via regulating microbiome remains unknown. Here, metagenomic and transcriptomic analysis were subsequently implemented to identify the Pb exposure-triggered prominent alternation of gut-liver signal. In the present study the severe intestinal injury and fatty liver formation caused by Pb in common carp were preliminarily determined. Metagenomic analysis confirmed that the gut microbiome dominant phyla, family and genus of the common carps were Fusobacteria , Fusobacteriaceae and Cetobacterium . Meanwhile, lipopolysaccharide (LPS) biosynthesis pathway was regarded as one of the main responsible for Pb exposure. Subsequently, LPS was demonstrated as the Pb-triggered microbial-derived signal of the common carps by ELISA analysis, and involves in the hepatic metabolic disorders via deteriorating the intestinal barrier. Additionally, it confirmed that hepatocytes ferroptosis associated with Pb-evoked fatty liver of the common carps, and the aggravation of lysosomal dyshomeostasis as well as inhibition of AMPK phosphorylation were referred to lipid metabolic disorders. The results of the present study demonstrated microbial-derived signal induced by aquatic Pb contaminant cause fatty liver formation in the common carps, and the protective effects of MT on Pb toxicity were performed by receding LPS over-synthesis, restraining microbiota-sourced LPS transport, along with attenuation of hepatocytes ferroptosis.
研究领域:
环境毒理学
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水生生物学
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分子生物学
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微生物学
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药理学
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产品关联
DOI
PubMed
高影响因子
Science Advances
·
2024
·Vol. 10
·期 23
·
IF 11.7
Bo Deng,Yue Ma,Jialyu Huang,Runbang He,Miaomiao Luo,Lina Mao,Enhua Zhang,Yuanyuan Zhao,Xiaoli Wang,Qiangsong Wang,Mingchang Pang,Yilei Mao,Huayu Yang,Lanxia Liu,Pengyu Huang
The utilization of three-dimensional (3D) bioprinting technology to create a transplantable bioartificial liver emerges as a promising remedy for the scarcity of liver donors. This study outlines our strategy for constructing a 3D-bioprinted liver, using in vitro–expanded primary hepatocytes recognized for their safety and enhanced functional robustness as hepatic cell sources for bioartificial liver construction. In addition, we have developed bioink biomaterials with mechanical and rheological properties, as well as printing capabilities, tailored for 3D bioprinting. Upon heterotopic transplantation into the mesentery of tyrosinemia or 90% hepatectomy mice, our 3D-bioprinted liver effectively restored lost liver functions, consequently extending the life span of mice afflicted with liver injuries. Notably, the inclusion of an artificial blood vessel in our 3D-bioprinted liver allowed for biomolecule exchange with host blood vessels, demonstrating, in principle, the rapid integration of the bioartificial liver into the host vascular system. This model underscores the therapeutic potential of transplantation for the treatment of liver failure diseases.
研究领域:
组织工程
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再生医学
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生物医学工程
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肝病学
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移植学
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DOI
PubMed
高影响因子
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