CARDIOVASCULAR DRUGS AND THERAPY
·
2024
·
IF 3.1
Ye Bozhi,Cai Xueli,Liang Xiaohe,Chen Yunxuan,Dai Shanshan,Huang Zhuqi,Huang Weijian,Zhang Lei,Wang Zixuan,Xing Jincheng,Lai Xianhui,Huang Zhouqing,Jia Zhuyin
Purpose Inflammatory responses induced by NLRP3 inflammasome contribute to the progression of atherosclerosis. This study seeks to investigate the effect of emodin on the NLRP3 inflammasome in atherogenesis and to probe the underlying mechanism. Methods ApoE-knockout (ApoE −/− ) mice were treated with a high-fat diet (HFD) for 12 weeks and intragastrically with emodin for 6 weeks. Human mononuclear cell line THP-1 was pretreated with emodin or signaling pathway inhibitors and induced into macrophages using phorbol 12-myristate 13-acetate (PMA) for 48 h. The NLRP3-mediated inflammatory response was studied both in vivo and in vitro. The level of the inflammation was detected by western blot, real-time PCR analysis, and ELISA. Results Emodin attenuated atherosclerotic lesions in HFD-treated ApoE −/− mice. Emodin dramatically decreased the expression of NLRP3, GSDMD, IL-1β, and IL-18 in HFD-treated ApoE −/− mice and PMA-induced macrophages. Moreover, emodin significantly hindered the activation of nuclear factor kappa-B (NF-κB) by inhibiting the formation of the TLR4/MyD88 complex in PMA-induced macrophages. Conclusion Our data demonstrate that emodin can inhibit the development of atherosclerotic plaques by alleviating NLRP3/GSDMD-induced inflammation through repressing the TLR4/MyD88/NF-κB signaling pathway in macrophages. This finding suggests that emodin can be a potential candidate for the treatment of atherosclerosis.
研究领域:
免疫学
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心血管疾病
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药理学
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DOI
PubMed
高影响因子
Advanced Science
·
2024
·
IF 14.3
Tao Xu,Hao Cheng,Hailiang Pei,Jiameng Wang,Yiwei Shi,Xiangyu Zhang,Di Huang
Eradication of osteomyelitis caused by bacterial infections is still a major challenge. Microwave therapy has the inherent advantage of deep penetration in curing deep tissue infections. However, the antibacterial efficiency of sensitizers is limited by the weak energy of microwaves. Here, a hybrid heterojunction system (Fe 3 O 4 /CuS/Emo) is designed for curing bacterially infected osteomyelitis. As an enhanced microwave sensitizer, it shows supernormal microwave response ability. Specifically, Fe 3 O 4 acts as a matrix to mediate magnetic loss. After CuS loading, the heterogeneous interface forms induce significant interfacial polarization, which increasing dielectric loss. On the basis of the heterojunction formed by the two semiconductors, emodin is innovatively introduced to modify it. This integration not only accelerates the movement of charge carriers but also enhances polarization loss due to the numerous functional groups present on the surface. This further optimizes the microwave thermal and catalytic response. In addition, the unique anti-inflammatory properties of emodin confer the ability of hybrid heterojunction to regulate the immune microenvironment. In vivo studies reveal that heterojunction modified by emodin programmed elimination of bacteria and regulation of the immune microenvironment. It offers a revolutionary approach to the treatment of bacterial osteomyelitis.
研究领域:
医学
·
材料科学
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产品关联
DOI
PubMed
高影响因子
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
·
2024
·
IF 2.5
Liuxuan Yang,Xianbin Liu,Jing Yang,Ke Wang,Zhenghao Ai,Jinlu Shang,Meiling Zhou
Acute pancreatitis (AP) is a severe inflammatory condition with a rising incidence and high mortality rates, especially in severe cases. Emodin (ED), known for its potent anti-inflammatory properties, holds promise in addressing AP. However, its clinical application is hindered by limitations such as low bioavailability and insufficient target specificity. Herein, we developed a novel drug delivery system using macrophage membrane-coated UiO-66-NH 2 nanoparticles loaded with ED (MVs-UiO-ED). UiO-66-NH 2 was successfully synthesized and characterized, revealing an octahedral structure with a suitable size distribution. The successful loading of ED onto UiO-66-NH 2 was confirmed by ultraviolet and infrared spectroscopy. Subsequently, MVs-UiO-ED was prepared by coating macrophage membrane-derived vesicles onto UiO-ED, resulting in a biomimetic delivery system. In vitro release studies demonstrated that MVs-UiO-ED exhibited a sustained-release profile, indicating its potential for prolonged drug circulation. An AP mouse model was established to evaluate the therapeutic efficacy of MVs-UiO-ED. Compared with the model group, MVs-UiO-ED significantly reduced serum levels of α-amylase and lipase, two indicators of pancreatitis severity. Furthermore, histopathological examinations revealed that MVs-UiO-ED ameliorated pancreatic tissue damage. This study underscores the potential of MVs-UiO-ED as an effective therapeutic approach for AP.
研究领域:
药理学
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纳米技术
·
炎症
·
药物递送系统
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产品关联
DOI
PubMed
高影响因子
PHYTOMEDICINE
·
2020
·
IF 4.268
Dan Wang,Minghui Sun,Ying Zhang,Zehong Chen,Shuya Zang,Genyun Li,Gao Li,Andrew R. Clark,Jiangeng Huang,Luqin Si
Background Ulcerative colitis (UC) is an intricate enteric disease with a rising incidence that is closely related to mucosa-barrier destruction, gut dysbacteriosis, and immune disorders. Emodin (1,3,8-trihydroxy-6-methyl-9,10-anthraquinone, EMO) is a natural anthraquinone derivative that occurs in many Polygonaceae plants. Its multiple pharmacological effects, including antioxidant, immune-suppressive, and anti-bacteria activities, make it a promising treatment option for UC. However, its poor solubility, extensive absorption, and metabolism in the upper gastrointestinal tract may compromise its anti-colitis effects. Purpose EMO was loaded in a colon-targeted delivery system using multifunctional biomedical materials and the enhanced anti-colitis effect involving mucosa reconstruction was investigated in this study. Methods EMO-loaded Poly (DL-lactide-co-glycolide)/Eudragit Ⓡ S100/montmorillonite nanoparticles (EMO/PSM NPs) were prepared by a versatile single-step assembly approach. The colon-specific release behavior was characterized in vitro and in vivo , and the anti-colitis effect was evaluated in dextran sulfate sodium (DSS)-induced acute colitis in mice by weight loss, disease activity index (DAI) score, colon length, histological changes, and colitis biomarkers. The integrity of the intestinal mucosal barrier was evaluated through transwell co-culture model in vitro and serum zonulin-related tight junctions and mucin2 (MUC2) in vivo . Results EMO/PSM NPs with a desirable hydrodynamic diameter (~ 235 nm) and negative zeta potential (~ -31 mV) could prevent the premature drug release (< 4% in the first 6 h in vitro ) in the upper gastrointestinal tract (GIT) and boost retention in the lower GIT and inflamed colon mucosa in vivo . Compared to free EMO-treatment of different doses in UC mice, the NPs could enhance the remedial efficacy of EMO in DAI decline, histological remission, and regulation of colitis indicators, such as myeloperoxidase (MPO), nitric oxide (NO), and glutathione (GSH). The inflammatory factors including induced nitric oxide synthase (iNOS), cyclooxygenase-2 (COX-2), TNF-α, and IL-1β were suppressed by EMO/PSM NPs at both mRNA and protein levels. The obtained NPs could also promote the regeneration of the mucosal barrier via reduced fluorescein isothiocyanate (FITC)-dextran leakage in the transwell co-culture model and decreased serum zonulin levels, which was demonstrated to be associated with the upregulated tight junctions (TJs)-related proteins (claudin-2, occludin, and zo-1) and MUC2 at mRNA level. Moreover, the NPs could contribute to attenuating the liver injury caused by free EMO under excessive immune inflammation. Conclusion Our results demonstrated that EMO/PSM NPs could specifically release EMO in the diseased colon, and effectively enhance the anti-colitis effects of EMO related to intestinal barrier improvement. It can be considered as a novel potential alternative for oral colon-targeted UC therapy by increasing therapeutic efficacy and reducing side-effects.
研究领域:
药学
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纳米技术
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胃肠病学
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免疫学
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材料科学
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DOI
PubMed
高影响因子
PHOTOCHEMICAL & PHOTOBIOLOGICAL SCIENCES
·
2020
·Vol. 19
·期 4
·485-494
·
IF 2.831
Ma Wenpeng,Liu Chengcheng,Li Jiao,Hao Ming,Ji Yanhong,Zeng Xiaoyan
The extensive and repetitive use of antifungal drugs has led to the development of drug-resistant Candida albicans . Antimicrobial photodynamic therapy (aPDT) has received considerable attention as an emerging and promising approach to combat drug-resistant microbes. This study evaluated the photodynamic effects mediated by aloe emodin (AE), a natural compound isolated from Aloe vera and Rheum palmatum, on azole-sensitive and azole-resistant C. albicans in vitro . AE exhibited no significant dark toxicity, but in the presence of light, effectively inactivated C. albicans cells in a concentration-dependent manner. The uptake of AE by fungal cells was investigated by confocal laser scanning microscopy (CLSM), and the results showed that AE possessed stronger ability to enter into C. albicans cells following light irradiation. Transmission electron microscopy analysis suggested that AE-mediated aPDT could induce damage to the cell wall, cytoplasm, and nucleus. Damage to the surface of C. albicans was observed by scanning electron microscopy. These results suggest that AE is a potential PS for use in aPDT of drug-resistant C. albicans strains, and AE-mediated aPDT shows promise as an antifungal treatment.
研究领域:
微生物学
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药理学
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抗菌治疗
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真菌病理学
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产品关联
DOI
PubMed
高影响因子
Cancer Cell International
·
2021
·Vol. 21
·期 1
·1-12
·
IF 5.722
Jiang Dongxiao,Ding Shufei,Mao Zhujun,You Liyan,Ruan Yeping
Background Colon cancer is a malignant gastrointestinal tumour with high incidence, mortality and metastasis rates worldwide. Aloe-emodin is a monomer compound derived from hydroxyanthraquinone. Aloe-emodin produces a wide range of antitumour effects and is produced by rhubarb, aloe and other herbs. However, the mechanism by which aloe-emodin influences colon cancer is still unclear. We hope these findings will lead to the development of a new therapeutic strategy for the treatment of colon cancer in the clinic.Methods We identified the overlapping targets of aloe-emodin and colon cancer and performed protein–protein interaction (PPI), Gene Ontology (GO), and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analyses. In addition, we selected apoptosis pathways for experimental verification with cell viability, cell proliferation, caspase-3 activity, DAPI staining, cell cycle and western blotting analyses to evaluate the apoptotic effect of aloe-emodin on colon cancer cells.Results The MTT assay and cell colony formation assay showed that aloe-emodin inhibited cell proliferation. DAPI staining confirmed that aloe-emodin induced apoptosis. Aloe-emodin upregulated the protein level of Bax and decreased the expression of Bcl-2, which activates caspase-3 and caspase-9. Furthermore, the protein expression level of cytochrome C increased in a time-dependent manner in the cytoplasm but decreased in a time-dependent manner in the mitochondria.Conclusion These results indicate that aloe-emodin may induce the apoptosis of human colon cancer cells through mitochondria-related pathways.
研究领域:
肿瘤学
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药理学
·
分子生物学
·
细胞生物学
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产品关联
DOI
PubMed
高影响因子
RSC Advances
·
2020
·Vol. 10
·期 35
·20862-20871
·
IF 3.119
Guoyan Ren,He Sun,Gen Li,Jinling Fan,Lin Du,Guoting Cui
The molecular mechanism of interaction between aloe-emodin (AE) and trypsin was investigated, exhibiting remarkable outcomes. To detect the interaction mechanism, the binding of AE with trypsin was examined by a multi-spectroscopy and molecular docking method. Results showed that the binding of AE and trypsin would lead to static quenching and their binding forces were van der Waals forces and hydrogen bonding. The results of simultaneous and three-dimensional fluorescence spectroscopy showed that the combination of AE and trypsin caused changes in the microenvironment around the trypsin fluorophore, which might change the spatial structure of trypsin. FT-IR spectroscopy showed that the contents of α-helix and β-turn in trypsin were decreased and the contents of β-sheet, random coil and antiparallel β-sheet were increased. Moreover, all these experimental results were verified and reasonably explained by molecular docking results. We also investigated the enzyme activity of trypsin and the antioxidant activity of AE. The results showed that both the enzyme activity of trypsin and the antioxidant activity of AE were decreased after interaction between AE and trypsin. The findings outlined in this study should elucidate the molecular mechanisms of interaction between AE and trypsin and contribute to making full use of AE in the food industry.
研究领域:
生物化学
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食品科学
·
药理学
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产品关联
DOI
PubMed
高影响因子
ACS Omega
·
2021
·
IF 3.512
Guodong Zheng,Jiahui Zheng,Le Xiao,Tongyi Shang,Yanjun Cai,Yuwei Li,Yiming Xu,Xiaoming Chen,Yun Liu,Bin Yang
In this study, a pH-responsive nano-prodrug was fabricated by conjugating emodin to the PEGylated polyethyleneimine (mPEG-PEI) with acid-sensitive boronate ester bonds. 1H NMR spectra results showed that emodin was effectively bonded to mPEG-PEI, and acid-sensitive assay further confirmed the formation of boronate ester bonds. The size and morphology of the nano-prodrug were ascertained through transmission electron microscopy (TEM) and dynamic light scattering (DLS), which showed that the prodrug has a sphere-like shape with hydrodynamic size around 102 nm at pH 7.4. Subsequently, a drug-release behavior assay was carried out to carefully investigate the acid-sensitive drug-delivery property of the prodrug. Moreover, in vitro cell viability assay confirmed the superior cytotoxic effect of the nano-prodrug against HeLa cells compared to free emodin. Furthermore, the antibacterial study showed that the nano-prodrug could inhibit the bacterial (both Gram-positive and Gram-negative) growth more effectively than free emodin. Overall, this study provides a promising paradigm of the multifunctional nano-prodrug for pH-responsive tumor therapy and antibacterial activity.
研究领域:
药剂学
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肿瘤学
·
微生物学
✓ 已验证
产品关联
DOI
PubMed
高影响因子
CHEMICO-BIOLOGICAL INTERACTIONS
·
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.
✓ 已验证
产品关联
DOI
PubMed
高影响因子
CHEMICAL ENGINEERING JOURNAL
·
2025
·
IF 13.2
Yuan Tian,Qing Xu,Ning Wang,Yanling Li,Wenyu Yang,Fei Huang,Qing Hao,Liping Zhao,Zhiruo Zhang,Fengchun Zhao,Fanglong Zhao
The intricate regulatory networks in filamentous fungi severely constrain the production of high-value natural products. Here, we developed an efficient CRISPR-dCas9-SunTag activation system to overcome transcriptional repression in Aspergillus nidulans . Through systematic optimization of GCN4 repeat numbers and implementation of P2A-mediated dCas9-SunTag/GCN4-VP64 tandem expression, this platform showed 20-fold higher activation efficiency compared to dCas9-VPR system. When deployed to regulate the emodin biosynthetic pathway, multiplexed sgRNA targeting enabled coordinated upregulation of three key biosynthetic genes mdpF , mdpG , and mdpH . This precise regulation approach minimized byproduct accumulation while boosting emodin titer to 101 mg/L, achieving 71 % higher production than the natural transcription factor overexpression. Furthermore, this optimized CRISPRa system demonstrated consistent stability during liquid fermentation in 1 L bioreactors (emodin 1.3 g/L) and solid-state fermentation (emodin 1.5 mg/g cell dry weight), highlighting its potential for scalable fungal metabolic engineering. This study establishes a modular and precise genetic toolkit for reprogramming fungal secondary metabolism, offering broad potential for the engineered biosynthesis of high-value compounds.
研究领域:
分子生物学
·
基因工程
·
合成生物学
·
真菌生物技术
·
天然产物生物合成
✓ 已验证
产品关联
DOI
高影响因子
INTERNATIONAL JOURNAL OF BIOLOGICAL MACROMOLECULES
·
2025
·
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
·
材料科学
·
分析化学
·
智能包装
·
环境监测
✓ 已验证
产品关联
DOI
PubMed
高影响因子
JOURNAL OF PHARMACOLOGICAL SCIENCES
·
2024
·
IF 3
Zhihang Zhang,Yalan Luo,Xijing Zhuang,Haifeng Gao,Qi Yang,Hailong Chen
Acute lung injury (ALI) is closely related to high mortality in severe acute pancreatitis (SAP). This study unveils the therapeutic effect and mechanism of miR-217-5p on SAP-associated ALI. The miR-217-5p RNA expression was significantly up-regulated in lipopolysaccharide (LPS)-stimulated primary rat alveolar epithelial type II cells (AEC II) and sodium taurocholate-treated pancreas and lung in SAP rats. miR-217 inhibition protected AEC II from LPS-induced damage by inhibiting apoptosis and reducing the TNF-α, IL-6, and ROS levels. miR-217 inhibition suppressed apoptosis and alleviated mitochondrial damage through mitochondria-mediated apoptotic pathway in vitro . Sirt1 is a direct target of miR-217-5p. Dual-luciferase reporter assay confirmed the binding of miR-217-5p to Sirt1 mRNA 3′-UTR. The rescue experiment identified that the anti-apoptotic, anti-inflammatory, and anti-oxidative effects of miR-217 inhibition were mediated by Sirt1 in vitro . Emodin (EMO) protected AEC II from LPS-induced damage and alleviated pancreatic and lung tissue injuries. EMO exerted similar effects as miR-217 inhibition in vitro and in vivo . The effects of EMO were abolished by miR-217 overexpression. In conclusion, miR-217-5p inhibition exerts protective effects on SAP-ALI in vitro and in vivo by repressing apoptosis, inflammation, and oxidative stress through Sirt1 activation. EMO protects against lung injuries in SAP-associated ALI rats through miR-217-5p/Sirt1 axis.
研究领域:
药理学
·
分子生物学
·
病理生理学
·
内科学
✓ 已验证
产品关联
DOI
PubMed
高影响因子
危险品化学品经营许可证（带存储）