INTERNATIONAL JOURNAL OF BIOLOGICAL MACROMOLECULES
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2025
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IF 8.5
Pan Liu,Hui Li,Kai Wang,Chuang Jiang,Xiyao Liang,Yuqing Zhang,Zhenyu Yu,Yaqing Xiao,Jinhui Zhou,Yingnan Liu
In this study, aloe emodin and β- d -glucose pentaacetate were added into potato starch/polyvinyl alcohol for the construction of colorimetric/fluorescent dual-pass intelligent response labels. Inspired by the lotus leaf structure, retained the advantages of the label itself and solved the hydrophilic problem of the label, and further developed a multi-functional dual-channel smart label with hydrophobicity and self-adhesion. The water contact angle of the prepared T-AEB label was 120.1 ± 0.8°, and the adhesion was 8 to 12 kPa. After burying T-AEB label in the soil for 35 days, the degradation rate reached 85 %, reflecting excellent ecological security. At pH (7–13) and volatile ammonia (25 to 25,000 ppm) conditions, the label's own color would change dramatically to indicate the effect. In sunlight, as the ammonia concentration increases, the color of the label changed from yellow to purplish red. Correspondingly, the fluorescent color of the label changed from yellow to blue. Under a 365 nm UV lamp. In addition, the label was successfully used for freshness monitoring of shrimp and razor clams during storage at 4 °C, 25 °C and − 20 °C. The smart label was a novel, economical, convenient and food freshness dual monitoring system, which was of great significance to improve food safety and quality monitoring.
研究领域:
食品科学
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材料科学
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分析化学
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智能包装
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环境监测
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PubMed
高影响因子
CHEMICO-BIOLOGICAL INTERACTIONS
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2026
·
IF 5.4
Lili Wu,Siyu Chen,Qiyuan Yang,Xing Li,Lingyan Liu,Shengjun Ji,Shuaiyuan Tang,Sihui Zhang,Yan Wang,Runzhi Chen,Zhikun Zhan
Emodin, a bioactive compound abundant in Chinese medicinal herbs, possesses broad therapeutic potential but raises safety concerns due to conflicting reports of hepatotoxicity. This study investigated the toxicological mechanisms underlying emodin-induced liver injury. Emodin (25-100 μM) elicited dose-dependent cytotoxicity in HepG2 cells, with the cytochrome P450 (CYP) enzymes CYP1A2 and CYP3A4 identified as the primary enzymes metabolizing emodin into hydroxylated products (M1-M3). The comparative cytotoxicity assay of emodin and its metabolites in HepG2 cells indicated that CYP-mediated metabolism functions as a critical detoxification pathway. Moreover, inhibition of CYP with 1-aminobenzotriazole (ABT, 500 μM) markedly enhanced emodin (12.5-100 μM) cytotoxicity in HepG2 cells. Similarly, ABT (50 mg/kg) markedly exacerbated emodin (400 mg/kg)-induced hepatotoxicity in mice following three weeks of co-administration. Transcriptomic profiling and validation experiments demonstrated that activation of the NF-κB/NLRP3 signaling axis contributes to emodin-induced hepatic injury. Metabolomic analyses further revealed perturbations in key pathways, including lipopolysaccharide (LPS) biosynthesis, sphingolipid metabolism, and cholesterol metabolism. Integrated multi-omics analysis identified a significant positive correlation between these metabolites (LPS, sphingosine, cholesterol) and NF-κB/NLRP3 pathway genes. These findings suggest that emodin-mediated upregulation of LPS, sphingosine, and cholesterol activates the NF-κB/NLRP3 pathway, subsequently triggering hepatic injury. Collectively, this study delineates the metabolic detoxification routes of emodin and provides mechanistic insight into its hepatotoxic potential.
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高影响因子
Frontiers in Pharmacology
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2017
·
IF 4.4
Jiang Li-Long,Zhao Dong-Sheng,Fan Ya-Xi,Yu Qiong,Li Ping,Li Hui-Jun
Polygoni Multiflori Radix (PMR) has been commonly used as a tonic in China for centuries. PMR-associated hepatotoxicity has been drawing increasingly more attention in recent years in parallel with its wide utilization. Anthraquinones (AQs) are recognized as the main hepatotoxic components in PMR. However, the exact underlying mechanism of AQs poisoning is still not fully understood. Herein, we proposed a hypothesis that metabolic activation of AQs such as emodin was involved in PMR-induced liver injury, AQs followed to generate the electrophilic reactive metabolites and subsequently formed covalent adduct with cellular nucleophiles in the liver to exert hepatotoxicity. In the present study, the link of cytotoxicity of PMR in primary human hepatocytes and the depletion of glutathione (GSH) was investigated by MTT assay and UHPLC-QqQ-MS/MS analysis. The results showed that PMR depleted GSH and therefore induced cytotoxicity. Then, emodin-GSH adduct was identified in bile of liver injured rats after intragastric administration of PMR or emodin with the aid of UHPLC-QTOF-MS/MS method. Our findings not only provided confirmative evidence that the mechanism of hepatotoxicity induced by AQs in PMR involved key metabolic steps, but also revealed that emodin-GSH adduct had potential to be further developed as a sensitive and traceable biomarker for the assessment of PMR-induced liver injury.
研究领域:
中药学
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毒理学
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分析化学
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PubMed
高影响因子
Molecular Medicine Reports
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2014
·Vol. 10
·期 2
·731-736
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IF 1.484
Jinghua Luo,Yong Yuan,Pengyu Chang,Dawei Li,Zhiqiang Liu,Yaqin Qu
The aim of the present study was to investigate the effects of aloe-emodin (AE) on the radiosensitivity and differentiation of HeLa human cervical cancer cells. Cell proliferation was assessed in the HeLa cervical cancer cell line by a methylthiazolyldiphenyl-tetrazolium bromide assay. Radiosensitivity was determined by a colony‑forming assay. Flow cytometry was used for analysis of cell cycle distribution and apoptosis. The expression of γ-H2AX and cyclin B was assessed by western blotting. Alkaline phosphatase (ALP) activity was measured by an ALP activity kit. It was demonstrated that AE inhibited the proliferation of HeLa cells in a concentration- and time-dependent manner, induced G2/M and S phase cell cycle arrest and enhanced the radiosensitivity of HeLa cells. The combination of AE and radiation induced apoptosis, upregulated cyclin B and γ-H2AX expression and further improved ALP activity compared with treatment with AE or radiation alone. AE enhanced the radiosensitivity of HeLa human cervical cancer cells in vitro, inhibited the proliferation of HeLa cells, induced G2/M phase cell cycle arrest and, in combination with radiation, induced the apoptosis and improved the differentiation of HeLa cells.
研究领域:
肿瘤学
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放射生物学
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药理学
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分子生物学
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DOI
PubMed
高影响因子
MOLECULAR PHARMACEUTICS
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2018
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IF 4.556
Lili Wu,Weichao Han,Yulian Chen,Tao Zhang,Junjin Liu,Shilong Zhong,Han Liu,Congcong Han,Zhongyi Zhang,Shuwen Liu,Lan Tang
Emodin is a main anthraquinone compound which exists in Chinese traditional medicines including Polygonum multiflorum and Rhubarb. It is documented to have obvious liver and kidney toxicity. This study aims to (a) estimate gender differences of the hepatotoxicity and toxicokinetics in rats after oral administration of emodin (60 and 150 mg/kg/d) for a consecutive 28 days and (b) clarify relative mechanisms caused by glucuronidation and disposition. Hepatotoxicity was significantly higher in female rats than that in male rats, as evidenced by histopathological and biochemical tests. Similarly, the toxicokinetic profiles of emodin have time and gender differences, which could cause time and gender differences in hepatotoxicity. The metabolic and transcriptomics data of 55 human liver and 36 human kidney samples demonstrated that UDP-glucuronosyltransferase 2B7 (UGT2B7) was the predominant enzyme for emodin glucuronidation. A genome-wide association study (GWAS) identified that rs11726899 located within ∼50 kb of the transcript of UGT2B could significantly affect emodin metabolism. Knockdown of UGT2B7 in HepG2 cells significantly decreased emodin glucuronidation and increased cytotoxicity of emodin. The gene expression and protein levels of UGT2B7 were decreased, but those of the multidrug-resistant-protein 2 (MRP2) were increased in HepG2 cells after being treated with 50 μM emodin for 48 h. Long-term use of emodin could decrease the intrinsic clearance (CLint, decreased by 18.5%–35.4%) values of zidovidue (UGT2B7 substrate) glucuronide in both male and female liver microsomes from rats administrated with emodin for 28 days, thus causing the accumulation of emodin. However, higher self-induced MRP2 expression and lower hepatotoxicity were observed in emodin-treated male rats compared to that in female rats. Therefore, gender differences in the hepatotoxicity and toxicokinetics of emodin are potentially mediated by the coupling of UGT2B7 and MRP2 in vivo.
研究领域:
药理学
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毒理学
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分子生物学
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高影响因子
JOURNAL OF BIOCHEMICAL AND MOLECULAR TOXICOLOGY
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2015
·Vol. 29
·期 11
·533-543
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IF 1.925
Xiaoyan Liu,Yanqiu Liu,Mengchun Cheng,Hongbin Xiao
ABSRACT The present study was undertaken to investigate the metabolic responses of human liver cells HL-7702 on chemicals purified from traditional Chinese medicine: emodin, triptolide, and aristolochic acid. Cytotoxicity tests demonstrated a dose-dependent toxic effect of emodin, triptolide, and aristolochic acid on HL7702 cells for 48 h. Emodin (14 μM), aristolochic acid (12 μg/mL), or triptolide (18 nM) was individually administrated to HL7702 and cell samples were collected after 48 h for metabolites extraction and analysis. Pattern recognition analysis reflected the significant difference in metabolic profiles between chemical-treated groups and the control group. Finally, eight metabolites including N 1 -acetylspermidine, Glu Gly, N -undecanoylglycine, C 16 sphinganine, sphinganine, glutathione, l -palmitoylcarnitine, and elaidic carnitine were detected as potential common biomarkers. Three pathways including sphinganine metabolism, fatty acid oxidation, and oxidative stress were identified. Our findings indicated that metabolomics would be an efficient approach to understand the molecular mechanism of hepatotoxicity induced by chemicals.
研究领域:
药理学
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毒理学
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代谢组学
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细胞生物学
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INTERNATIONAL JOURNAL OF PHARMACEUTICS
·
2016
·
IF 3.994
Tianpeng Zhang,Dong Dong,Danyi Lu,Shuai Wang,Baojian Wu
Oral emodin , a natural anthraquinone and active component of many herbal medicines, is poorly bioavailable because of extensive first-pass glucuronidation. Here we aimed to prepare emodin nanoemulsion (EMO-NE) containing cremophor EL , and to assess its potential for enhancing transcellular absorption of emodin using UGT1A1-overexpressing MDCKII cells (or MDCK1A1 cells). EMO-NE was prepared using a modified emulsification technique and subsequently characterized by particle size, morphology, stability, and drug release. MDCKII cells were stably transfected with UGT1A1 using the lentiviral transfection approach. Emodin transport and metabolism were evaluated in Transwell-cultured MDCK1A1 cells after apical dosing of EMO-NE or control solution. The obtained EMO-NE (116 ± 6.5 nm) was spherical and stable for at least 2 months. Emodin release in vitro was a passive diffusion-driven process. EMO-NE administration increased the apparent permeability of emodin by a 2.3-fold ( p < 0.001) compared to the pure emodin solution (1.2 × 10 −5 cm/s vs 5.3 × 10 −6 cm/s). Further, both apical and basolateral excretion of emodin glucuronide (EMO-G) were significantly decreased (≥ 56.5%, p < 0.001) in EMO-NE group. This was accompanied by a marked reduction (57.4%, p < 0.001) in total emodin glucuronidation. It was found that the reduced glucuronidation was due to inhibition of cellular metabolism by cremophor EL. Cremophor EL inhibited UGT1A1-mediated glucuronidation of emodin using the mixed-type inhibition mechanism. In conclusion, cremophor EL-based nanoemulsion greatly enhanced transcellular permeation of emodin through inhibition of UGT metabolism. This cremophor EL-based nanoformulation may be a promising strategy to improve the oral bioavailability of emodin.
研究领域:
药理学
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药物递送系统
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细胞生物学
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DOI
PubMed
高影响因子
Frontiers in Microbiology
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2021
·
IF 5.64
Cui Zixin,Zhang Miaomiao,Geng Songmei,Niu Xinwu,Wang Xiaopeng,Zhu Yanyan,Ye Feng,Liu Chengcheng
Infectious dermatological diseases caused by Malassezia furfur are often chronic, recurrent, and recalcitrant. Current therapeutic options are usually tedious, repetitive, and associated with adverse effects. Alternatives that broaden the treatment options and reduce side effects for patients are needed. Antimicrobial photodynamic therapy (aPDT) is an emerging approach that is quite suitable for superficial infections. The aim of this study is to investigate the antimicrobial efficacy and effect of aPDT mediated by haematoporphyrin monomethyl ether (HMME) and aloe emodin (AE) on clinical isolates of M. furfur in vitro. The photodynamic antimicrobial efficacy of HMME and AE against M. furfur was assessed by colony forming unit (CFU) assay. The uptake of HMME and AE by M. furfur cells was investigated by fluorescence microscopy. Reactive oxygen species (ROS) probe and flow cytometry were employed to evaluate the intracellular ROS level. The effect of HMME and AE-mediated aPDT on secreted protease and lipase activity of M. furfur was also investigated. The results showed that HMME and AE in the presence of light effectively inactivated M. furfur cells in a photosensitizer (PS) concentration and light energy dose-dependent manner. AE exhibited higher antimicrobial efficacy against M. furfur than HMME under the same irradiation condition. HMME and AE-mediated aPDT disturbed the fungal cell envelop, significantly increased the intracellular ROS level, and effectively inhibited the activity of secreted protease and lipase of M. furfur cells. The results suggest that HMME and AE have potential to serve as PSs in the photodynamic treatment of dermatological diseases caused by M. furfur, but further ex vivo or in vivo experiments are needed to verify that they can meet the requirements for clinical practice.
研究领域:
皮肤科
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光生物学
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微生物学
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药学
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CANADIAN JOURNAL OF PHYSIOLOGY AND PHARMACOLOGY
·
2015
·Vol. 93
·期 6
·
IF 1.77
Feng Cao,Wei Peng,Xiaoli Li,Ming Liu,Bin Li,Rongxin Qin,Weiwei Jiang,Yanyan Cen,Xichun Pan,Zifei Yan,Kangkang Xiao,Hong Zhou
This study investigated the anti-methicillin-resistant Staphylococcus aureus (anti-MRSA) activity and chemical compositions of ether extracts from Rhizoma Polygoni Cuspidati (ET-RPC). Significant anti-MRSA activities of ET-RPC against MRSA252 and MRSA clinical strains were tested in in vitro antibacterial experiments, such as inhibition zone diameter test, minimal inhibitory concentration test, and dynamic bacterial growth assay. Subsequently, 7 major compounds of ET-RPC were purified and identified as polydatin, resveratrol-4-O-d-(6′-galloyl)-glucopyranoside, resveratrol, torachryson-8-O-glucoside, emodin-8-O-glucoside, 6-hydroxy-emodin, and emodin using liquid chromatography – electrospray ionization – tandem mass spectrometry. After investigation of anti-MRSA activities of the 7 major compounds, only emodin had significant anti-MRSA activity. Further, transmission electron microscopy was used to observe morphological changes in the cell wall of MRSA252, and the result revealed that emodin could damage the integrity of cell wall, leading to loss of intracellular components. In summary, our results showed ET-RPC could significantly inhibit bacterial growth of MRSA strains. Emodin was identified as the major compound with anti-MRSA activity; this activity was related to destruction of the integrity of the cell wall and cell membrane.
研究领域:
微生物学
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药理学
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DOI
PubMed
高影响因子
Asian Pacific Journal of Cancer Prevention
·
2014
·Vol. 15
·期 13
·5201-5205
·
IF 1.5
Xie Mei-Juan,Ma Yi-Hua,Miao Lin,Wang Yan,Wang Hai-Zhen,Xing Ying-Ying,Xi Tao,Lu Yuan-Yuan
Emodin, a natural anthraquinone isolated from the traditional Chinese medicine Radix rhizoma Rhei, can induce apoptosis in many kinds of cancer cells. This study demonstrated that emodin induces apoptosis in human colon cancer HCT116 cells by provoking oxidative stress, which subsequently triggers a p53-mitochondrial apoptotic pathway. Emodin induced mitochondrial transmembrane potential loss, increase in Bax and decrease in Bcl-2 expression and mitochondrial translocation and release of cytochrome c to cytosol in HCT116 cells. In response to emodin-treatment, ROS increased rapidly, and subsequently p53 was overexpressed. Pretreatment with the antioxidant NAC diminished apoptosis and p53 overexpression induced by emodin. Transfecting p53 siRNA also attenuated apoptosis induced by emodin, Bax expression and mitochondrial translocation being reduced compared to treatment with emodin alone. Taken together, these results indicate that ROS is a trigger of emodin-induced apoptosis in HCT116 cells, and p53 expression increases under oxidative stress, leading to Bax-mediated mitochondrial apoptosis.
研究领域:
肿瘤学
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细胞生物学
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药理学
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DOI
PubMed
高影响因子
JOURNAL OF CONTROLLED RELEASE
·
2026
·
IF 12.4
Linxin Dai,Qian Wang,Lingling He,Ziyu Yuan,Fenglian Zhang,Ruifeng Luo,Lingqiang Li,Wenzhen Zhong,Yan Ye,Wen Li,Chaomei Fu,Peng Zhao,Runchun Xu,Chuan Zheng,Ruibing Wang,Fei Gao
While mucosal layer restoration is one of the key therapeutic goals for ulcerative colitis (UC), the current clinical treatments, including probiotics and therapeutic agents, fail to achieve it. As mucosal integrity often depends on goblet cell (GC) abundance and mucus secretion capability, herein we developed LEG@PDA, an orally delivered probiotics-nanotherapeutic system, composed of Lactobacillus rhamnosus GG (LGG) backpacked with emodin-loaded lactoferrin nanoparticles (LENs) and surface-coated with polydopamine (PDA). The outer layer PDA provides gastric protection and colon-targeted delivery, while LENs exhibit lactoferrin-mediated targeting to colonic epithelial cells, concurrently suppressing ferroptosis through iron homeostasis modulation, mitochondrial stabilization, and GSH-GPX4 axis activation. This significantly increases GC population, providing a cellular reservoir for enhanced mucus secretion. Simultaneously, LGG is delivered to colonic patches through M cell-mediated transcytosis, where it orchestrates mucus extrusion of GC via the CGRP-RAMP1 axis. In murine models, LEG@PDA exhibited excellent efficacy in UC management and preventing disease relapse. This strategy, combining probiotics and natural compound-loaded nanobackpacks, offers a practical and targeted approach to restore the GC-dependent mucosal layer via Colonic patches, presenting a promising advance for effective UC treatment.
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Drug Design Development and Therapy
·
2025
·
IF 5.1
Yujun Chen,Yuhang Zhao,Qing Wang,Qiuchi Chen,Xiqun Chen,Kai Yang
Background Parkinson’s disease (PD) is a common neurodegenerative disorder. Emodin (EMD), which is derived from multiple Chinese medicinal herbs, has been reported to possess anti-inflammatory, anti-ferroptosis, and neuroprotective effects. However, the mechanisms underlying the regulation of PD-related ferroptosis remain unclear.Objective To investigate whether EMD protects dopaminergic neurons in 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced models of PD and to elucidate its underlying mechanisms.Methods Potential EMD targets were predicted using SEA and Swiss databases. The PD targets were identified using the OMIM and GeneCards databases. Overlapping genes were introduced to construct protein-protein interactions (PPI) and perform Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analyses. Molecular docking was used to ascertain the possibility of the binding of EMD to p53 and TfR1. The stability of EMD-p53 complex was validated by using molecular dynamics simulations using the YASARA. To validate these mechanisms, we used an MPTP-induced mouse model to investigate the beneficial effects of EMD. Motor function was assessed using the open field and rotarod tests. Malondialdehyde (MDA) and iron contents in the midbrain were determined. SH-SY5Y cells were subjected with 1-methyl-4-phenyl-pyridinium (MPP+) or ferroptosis inducer. Ferroptosis signaling, iron metabolism, and mitochondrial superoxide levels were investigated using Western blotting, qPCR, immunofluorescence, and flow cytometry.Results Enrichment analysis revealed that the shared targets of the PD and EMD gene sets were involved in iron metabolism, with TP53 being the most connected protein in the PPI network. Molecular docking analysis suggested that EMD formed a stable complex with p53 or TfR1. Molecular Dynamics Simulation further confirmed that the interactions between EMD and p53 remained stable over time. In vivo studies demonstrated the beneficial effects of EMD in an MPTP mouse model of PD. This action was achieved by inhibiting p53 expression and mitigating ferroptosis signaling in the substantia nigra (SN). EMD similarly attenuated cell injury and ferroptosis in SH-SY5Y cells by inhibiting p53-ferroptosis signaling. In contrast, pharmacological enhancement of p53 nullified these effects in the MPP+-treated SH-SY5Y cells.Conclusion These preliminary results indicate that EMD could exert neuroprotective effects against MPTP-induced toxicity, possibly via modulating p53-ferroptosis signaling.
研究领域:
神经科学
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药理学
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分子生物学
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中医药学
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计算生物学
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PubMed
高影响因子
危险品化学品经营许可证（带存储）