Journal of Environmental Chemical Engineering
·
2023
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IF 7.7
Jiajia Li,Yi Li,Mengzhen Zhu,Qiong Mei,Xi Tang,Yao Wu,Shijun Yue,Yuping Tang,Qizhao Wang
Photocatalysis-Fenton degradation of antibiotic pollutants is an attractive avenue, but its practical application is limited by easy recombination of photocarriers and low efficiency of Fe 3+ /Fe 2+ cycling. This work intends to introduce aloe-emodin into FeOOH with the purpose of improving the carrier separation rate by organic-inorganic heterojunction , as well as promoting the iron cycle (Fe 3+ /Fe 2+ ) transformation and inhibiting Fe 3+ precipitation in photocatalysis-Fenton through its complexation and reducibility, so as to achieve efficient degradation of antibiotic pollutants. Conspicuously, the prepared aloe-emodin/FeOOH sample showed nearly 85% tetracycline (TC) removed within 1 h with visible light and H 2 O 2 , which was almost 2.02 and 2.12 times larger than those of aloe-emodin and FeOOH, separately. The superior degradation performance ascribed to the synergistic effect of the aloe-emodin and FeOOH in the presence of H 2 O 2 as a strong oxidant. Moreover, the paper is focused on the effects of aloe-emodin/FeOOH interface structural characteristics on transmission modes of carriers and surface catalytic kinetics. The generated •OH, •O 2 − and 1 O 2 could serve as the active species achieving relatively high efficiency of Fe 3+ /Fe 2+ cycling and rapidly photogenerated charge separation in the degradation progress. Finally, we have tried to illustrate the internal mechanism of photocatalysis-Fenton treatment of antibiotic pollutants by aloe-emodin/FeOOH. Additionally, these investigations will provide practical and technical support for further exploitation of similar organic-inorganic photocatalysts, which is expected to accelerate the development of photocatalysis-Fenton degradation in the field of environmental purification.
研究领域:
环境科学
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材料科学
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化学工程
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DOI
高影响因子
ACS Biomaterials Science & Engineering
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2018
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IF 4.432
Juqun Xi,Qiuwen Wu,Zhilong Xu,Yanqiu Wang,Beibei Zhu,Lei Fan,Lizeng Gao
Development of effective antimicrobial wound dressings has drawn wide attention in the wound care market. Here, we synthesized a natural antibiotic (aloe-emodin, AE) and a carbon nanoparticle coembedded polymer hybrid hydrogel as a novel wound dressing in the fight against potent skin infections. We systematically evaluated the properties of the obtained hydrogels, including physico-chemical characteristics, photothermal conversion efficiency, reactive oxygen species (ROS) generation, AE-released profile, antibacterial activity, and wound-healing capability. The hybrid gels can initially reduce the number of bacteria in a short time through the near-infrared-light (NIR) triggered photothermal/ROS route and continuously kill the remaining live cells by releasing AE from gels after turning off the NIR source with a long-term antibacterial effect. These two antibacterial mechanisms that complement each other lead to excellent antibacterial performance toward various bacterial strains including multidrug-resistant bacteria. Moreover, in vivoStaphylcoccus aureus-infected animal experiments indicate that the hybrid gels upon NIR irradiation have a striking ability toward wound infection. These studies demonstrate that the AE and carbon nanoparticle coembedded hybrid polymer hydrogels with NIR exposure may have applications in wound combined care for bacterial infections.
研究领域:
材料科学
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生物医学工程
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药剂学
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微生物学
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PubMed
高影响因子
Nutrients
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2022
·Vol. 14
·期 13
·2768
·
IF 6.706
Di Chen,Jiyong Yin,Zhuo Yang,Wen Qin,Junsheng Huo,Jian Huang,Jing Sun,Wei Piao
The current cytological evaluation technique of health food raw materials does not entirely meet the needs of evaluating health food. Our study adopted the microfluidic chip technique for the first time to construct a hepatocyte model of evaluating emodin, which was composed of a human hepatocellular carcinoma cell (HepG2) and microfluidic chip. The mixed glue of a model with rat tail collagen type I (1.3 mg/mL) + gelatin (7.5%) was used to simulate the microenvironment of a cell. The validity of this model was evaluated by cell proliferation activity and cell staining, and the toxicity of emodin was evaluated by a series of metabolic indicators on this model. The results indicated that the repeatability of the constructed hepatocyte model was favorable, with a coefficient of variation (CV) of 2.8%. After emodin continuously was exposed for 48 h, the cell inhibition was obvious at 100 and 200 μM, and the number of dead cells gradually increased with the increasing of emodin concentration, and the difference of BUN was significant between the emodin group and blank group (p< 0.05). The constructed model has a favorable applicability in evaluating emodin. This study provides an important platform and a potential in vitro alternative model for assessing and predicting the health effects of health food.Keywords:microfluidic chip;raw materials of health food;emodin;hepatocyte model;evaluation
研究领域:
生物技术
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毒理学
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药理学
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PubMed
高影响因子
Drug Design Development and Therapy
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2022
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IF 4.319
Bozhi Ye,Xudong Chen,Shanshan Dai,Jibo Han,Xiaohe Liang,Shuang Lin,Xueli Cai,Zhouqing Huang,Weijian Huang
Background Emodin has recently been reported to have a powerful antiinflammatory effect, protecting the myocardium against ischemia/reperfusion (I/R) injury. Pyroptosis is a proinflammatory programmed cell death that is related to many diseases. The present study investigated the effect of emodin on pyroptosis in cardiomyocytes.Materials and methods Sprague Dawley rats were randomly divided into sham, I/R, and I/R+Emodin groups. I/R model was subjected to 30 minutes’ ligation of left anterior descending coronary artery, followed by 2 hours of reperfusion. Cardiomyocytes were exposed to hypoxic conditions for 1 hour and normoxic conditions for 2 hours. The level of the pyroptosis was detected by Western blot, real-time PCR analysis, and ELISA.Results The level of gasdermin D-N domains was upregulated in cardiomyocytes during I/R or hypoxia/reoxygenation (H/R) treatment. Moreover, emodin increased the rate of cell survival in vitro and decreased the myocardial infarct size in vivo via suppressing the levels of I/R-induced pyroptosis. Additionally, the expression of TLR4, MyD88, phospho-IκBα, phospho-NF-κB, and the NLRP3 inflammasome was significantly upregulated in cardiomyocytes subjected to H/R treatment, while emodin suppressed the expression of these proteins.Conclusion This study confirms that emodin treatment was able to alleviate myocardial I/R injury and inhibit pyroptosis in vivo and in vitro. The inhibitory effect of emodin on pyroptosis was mediated by suppressing the TLR4/MyD88/NF-κB/NLRP3 inflammasome pathway. Therefore, emodin may provide an alternative treatment for myocardial I/R injury.
研究领域:
药理学
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心脏病学
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细胞生物学
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分子生物学
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PubMed
高影响因子
JOURNAL OF BIOCHEMICAL AND MOLECULAR TOXICOLOGY
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2022
·Vol. 37
·期 1
·e23229
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IF 3.568
He-Yu Yang,Ji Wu,Hong Lu,Meng-Lin Cheng,Bang-Hua Wang,Hai-Li Zhu,Ling Liu,Min Xie
Oxaliplatin (OXA) is a common chemotherapy drug for colorectal, gastric, and pancreatic cancers. The anticancer effect of OXA is often accompanied by neurotoxicity and acute and chronic neuropathy. The symptoms present as paresthesia and pain which adversely affect patients' quality of life. Herein, five consecutive intraperitoneal injections of OXA at a dose of 4 mg/kg were used to mimic chemotherapy. OXA administration induced mechanical allodynia, activated spinal astrocytes, and increased inflammatory response. To develop an effective therapeutic measure for OXA-induced neuropathic pain, emodin was intrathecally injected into OXA rats. Emodin developed an analgesic effect, as demonstrated by a significant increase in the paw withdrawal threshold of OXA rats. Moreover, emodin treatment reduced the pro-inflammatory cytokines (tumor necrosis factor-α and interleukin-1β) which upregulated in OXA rats. Furthermore, autodock data showed four hydrogen bonds were formed between emodin and cyclooxygenase-2 (COX2), and emodin treatment decreased COX2 expression in OXA rats. Cell research further proved that emodin suppressed nuclear factor κB (NF-κB)-mediated inflammatory signal and reactive oxygen species level. Taken together, emodin reduced spinal COX2/NF-κB mediated inflammatory signal and oxidative stress in the spinal cord of OXA rats which consequently relieved OXA-induced neuropathic pain.
研究领域:
药理学
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神经科学
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炎症
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疼痛管理
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癌症治疗
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DOI
PubMed
高影响因子
INTERNATIONAL IMMUNOPHARMACOLOGY
·
2023
·
IF 5.6
Chen Wang,Lulu Wu,Runjin Zhou,Cuiwen Song,Peng Chen,Shiying Huang,Ahsan Ali Khan,Deng Lu,Yong Hu,Lukui Chen
Background and objective Neuropathic pain (NeP) induced dysbiosis of intestinal microbiota in chronic constriction injury (CCI) rats. Emodin has analgesic effect but the detailed mechanism is not clear at the present time. This study aims to explore the underling mechanism of action of emodin against NeP with in CCI model. Methods Male SD rats (180–220 g) were randomly divided into three groups: sham group, CCI group, and emodin group. Behavioral tests were performed to evaluate the therapeutic effects of emodin on CCI model. Feces and spinal cords of all rats were collected 15 days after surgery. 16S rDNA sequencing, untargeted metabolomics, qPCR and ELISA were performed. Results Mechanical withdrawal thresholds (MWT), thermal withdrawal latency (TWL) and Sciatic functional index (SFI) in emodin group were significantly higher than CCI group (P < 0.05). Emodin not only inhibited the expression of pro-inflammatory cytokines in the spinal cords and colonic tissue, but also increased the expression of tight junction protein in colonic tissue. 16S rDNA sequencing showed that emodin treatment changed the community structure of intestinal microbiota in CCI rats. Untargeted metabolomics analysis showed that 33 differential metabolites were screened out between CCI group and emodin group. After verification, we found that emodin increased the level of S-adenosylmethionine (SAM) and Histamine in the spinal cord of CCI rats. Conclusion Emodin was effective in relieving neuropathic pain, which is linked to inhibition inflammatory response, increasing the proportion of beneficial bacteria and beneficial metabolites.
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高影响因子
INTERNATIONAL IMMUNOPHARMACOLOGY
·
2024
·
IF 4.8
Jinsheng Gao,Yousong Li,Jiaohua Chen,Wen Feng,Jianchen Bu,Zixuan Lu,Jiandong Wang
Background Emodin, a natural anthraquinone derivative isolated from the roots of Rheum officinale Baill, has many pharmacological effects including anti-inflammatory, antioxidant, antiviral, antibacterial and anti-cancer. However, little is known about the effect of emodin on acute radiation proctitis (ARP). The present study was conducted to determine its effects and elucidate its mechanisms involving AKT/MAPK/NF-κB/VEGF pathways in ARP mice. Methods Total 60 C57BL/6 mice were divided randomly into control group, ARP group, AKT inhibitor MK-2206 group, and different doses of emodin groups. ARP mice were induced by 27 Gy of 6 MV X-ray pelvic local irradiation. MK-2206 was given orally for 2 weeks on alternate days. Emodin was administered daily by oral gavage for 2 weeks. Subsequently, all mice were sacrificed on day 15. The rectal tissues were obtained for further tests. The general signs score and the pathological grade were used to evaluate the severity of ARP. The expression of NF-κB, VEGF and AQP1 were determined by immunohistochemistry and western blot. The expression of p-AKT, p-ERK, p-JNK, p-p38, Bcl-2 and Bax were assessed using western blot. Results The worse general signs and damaged tissue structure of ARP mice were profoundly ameliorated by emodin. The expression of p-AKT, p-ERK, NF-κB, VEGF and AQP1 were significantly increased, resulting in the inflammation-induced angiogenesis in ARP mice. However, the expression of p-JNK and p-p38 were decreased, leading to the reduction of apoptosis in ARP mice. Excitedly, emodin reversed these changes, not only inhibited inflammation-induced angiogenesis, but also promoted apoptosis. Notably, the effects of emodin were similar to that of AKT inhibitor MK-2206, suggesting the involvement of AKT signaling in the effect of emodin. Conclusion These results suggest that emodin attenuates ARP in mice, and the underlying mechanism might involve inhibition of the AKT/ERK/NF-κB/VEGF pathways and the induction of apoptosis mediated by JNK and p38.
研究领域:
药理学
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放射生物学
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分子生物学
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炎症研究
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癌症研究
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DOI
PubMed
高影响因子
Life-Basel
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2025
·Vol. 15
·期 12
·1920
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IF 3.4
Chenliang Chu,Liang Qin,Huayong Peng,Tao Kuang,Yongshi Li,Xin Wang,Fenglan Liang,Ping Gao,Xiaoxiong Wang,Deyun Ma
Methicillin-resistantStaphylococcus aureus(MRSA) poses a significant clinical challenge due to its multidrug resistance, particularly to β-lactam antibiotics. This study comprehensively evaluated the natural compound emodin for its anti-MRSAactivity, mechanisms of action, and potential for synergy with β-lactam antibiotics. Our findings demonstrate that emodin dose-dependently inhibitsMRSAgrowth and abrogates biofilm formation at 2× MIC. Mechanistic studies revealed that emodin compromises cell membrane and wall integrity, induces oxidative stress, and downregulates the virulence factors SPA and EsxA. Furthermore, emodin acted synergistically with β-lactam antibiotics: it enhanced the ability of cefalexin to block bacterial adhesion and invasion of HaCat cells, and potentiated the efficacy of amoxicillin in clearingMRSAfrom infected macrophages. In conclusion, emodin employs a multi-target mechanism againstMRSAand can resensitize the bacterium to conventional β-lactam antibiotics, presenting a promising strategy for combination therapy that may help curb antibiotic use and resistance development.
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高影响因子
EUROPEAN FOOD RESEARCH AND TECHNOLOGY
·
2026
·Vol. 252
·期 7
·280
·
IF 4.2
Pan Shenrui,Wu Jiali,Liu Dan,Sun Jianxia,Bai Weibin
Aloe-emodin (AE), a natural photosensitizer, suffers from poor aqueous solubility that limits its photodynamic efficacy. This study developed a novel food-friendly co-amorphous system using ferulic acid (FA) as a co-former to enhance AE’s solubility and photodynamic performance. The AE-FA co-amorphous mixture was characterized by powder X-ray diffraction (PXRD), differential scanning calorimetry (DSC), and Fourier-transform infrared spectroscopy (FTIR) with molecular dynamics simulations confirming hydrogen bond formation. Results demonstrated that this complexation effectively reduced the lattice energy of AE, leading to significantly improved solubility and physical stability of the CAM system. Furthermore, AE-FA CAM exhibited enhanced antimicrobial photodynamic activity against Staphylococcus aureus compared to pure AE, which was attributed to reduced molecular agglomeration and alleviated fluorescence quenching. This study aims to develop a novel, food-friendly co-amorphous system to simultaneously enhance the solubility and photodynamic efficacy of AE. This work presents the first report of a co-amorphous system between AE and FA specifically designed for photodynamic applications, providing an effective strategy to overcome solubility limitations of natural photosensitizers in food safety applications.
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高影响因子
NANO
·
2025
·
IF 1.1
Wenlin Zhou,Qing Guo,Fangzhou Wen,Zongyan Chen,Lini Huo,Peiyuan Li
Bacteria are among the main causes of various diseases, which makes the search for safe and effective antimicrobial agents a major focus of research. In this study, nanocarbon quantum dots (Emo-CDs) with photodynamic antimicrobial activity were synthesized from rhodopsin (Emo) and β -cyclodextrin ( β -CD) using a simple hydrothermal method. This system, when combined with photodynamic therapy (PDT), exhibited enhanced antimicrobial properties. The prepared Emo-CDs can efficiently generate singlet oxygen under light irradiation, meeting the requirements for photodynamic antimicrobial activity. The antimicrobial efficacy of Emo-CDs was found to be concentration-dependent. After 10 min of xenon lamp irradiation, Emo-CDs demonstrated significantly greater antibacterial activity than Emo alone, achieving bactericidal rates as high as 99.89% against S. aureus and 97.75% against E. coli . Additionally, the photodynamic bactericidal effect increased with higher concentrations of Emo-CDs. Moreover, the system showed stable photoluminescence and good biocompatibility. In conclusion, the Emo-CDs system demonstrates great potential for improving the bioavailability, biocompatibility and antimicrobial efficacy of Emo, providing new strategies for developing novel dosage forms of active compounds in traditional Chinese medicine.
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DOI
高影响因子
INFLAMMATION RESEARCH
·
2026
·Vol. 75
·期 1
·37
·
IF 6.2
Wang Rui,Zou Ziwei,An Yi,Wang Liulin,Li Chengyin,Zou Yinshui,Wang Guangzhi
Background Acute kidney injury (AKI), characterized by rapid renal dysfunction and high mortality, is critically driven by ferroptosis, an iron-dependent form of cell death. While PTEN-induced kinase 1 (PINK1) and sirtuin 3 (SIRT3) are implicated in mitochondrial homeostasis and ferroptosis regulation, their mechanistic interplay in AKI remains unclear. This study investigated the role of emodin, a natural anthraquinone, in alleviating AKI via SIRT3-mediated PINK1 deacetylation and ferroptosis suppression, focusing on mitochondrial integrity, transferrin (TF) interaction, and redox balance. Materials and methods Male C57BL/6 mice ( n = 6/group), PINK1⁻/⁻, and SIRT3⁻/⁻ mice were pretreated with emodin (40–160 mg/kg, 3 days) before LPS-induced AKI (15 mg/kg). Human renal tubular HK-2 cells were treated with emodin (10–40 µg/ml) and Erastin (0.4 µM, 24 h). Assays included RNA sequencing, immunoprecipitation-mass spectrometry (IP-MS), histopathology (H&E/PAS/PB-DAB staining), ROS/Fe²⁺/GSH quantification, and immunoblotting. Statistical analysis used ANOVA and Student’s t-test. Results Emodin reduced serum creatinine and urea in AKI mice, alongside decreased tubular injury and apoptosis. RNA-seq identified ferroptosis as the central pathway, with emodin upregulating PINK1 expression. IP-MS revealed emodin disrupted PINK1-TF binding via SIRT3-mediated deacetylation, reducing Fe²⁺ accumulation and restoring GPX4 levels. In SIRT3⁻/⁻ and PINK1⁻/⁻ models, emodin’s protective effects were abolished, confirming pathway dependency. Conclusion Emodin mitigates AKI by activating the SIRT3/PINK1 axis, suppressing ferroptosis through cytoplasmic PINK1 deacetylation and TF interaction disruption. These findings highlight SIRT3/PINK1 as a therapeutic target and emodin as a potential agent for AKI management.
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PubMed
高影响因子
PHYTOMEDICINE
·
2025
·
IF 8.3
Jun Wang,Yongzheng Liu,Chongxiang Sun,Long Chen,Sikai Chen,Xingyu Huang,Zhijia Lu,Chunliu Dong,Yadan Zheng,Zhiyun Zhang,Yanyan Liu,Qianwei Qu,Yanhua Li
Background : Streptococcus suis is a zoonotic pathogen that causes meningitis, septicaemia, endocarditis, arthritis, and pneumonia in human beings. With the increasing prevalence of S. suis infections and a general decline in the effectiveness of antibiotics, the development of novel drugs that have effect on S. suis is extremely urgent. Emodin, a natural anthraquinone derivative of Rheum palmatum L., Reynoutria japonica Houtt., Polygonum multiflorum Thunb. and Cassia obtusifolia L., has been reported to exert anti- S. suis effect; however, the specific mechanism of the anti- S. suis action by targeting β-ketoacyl-acyl carrier protein synthase Ⅱ (FabF) in the fatty acid synthesis pathway remains unexplored. Purpose: We sought to reveal the potential role of emodin to prevent S. suis infection, investigate its mechanism of anti- S. suis action, and provide further evidence of emodin as an alternative to traditional antibiotic agents. Methods : The in vitro anti- S. suis properties of emodin were assessed through minimum inhibitory concentration (MIC) assays, and time-kill assays. Subsequently, the mechanisms underlying emodin’s mode of action at the molecular level by targeting FabF were elucidated using molecular docking, site-directed mutagenesis, bio-layer interferometry assays, and cellular thermal shift assays. Finally, metabolomics, cell membrane phospholipid content assay and biochemical parameters assays were used to detect emodin disrupting cell membrane integrity and function by affecting fatty acid biosynthesis. Results : In this study, we have identified that emodin inhibits S. suis by suppressing free fatty acids (FFAs) synthesis and disrupting phospholipid production by targeting FabF, a key enzyme in the fatty acid biosynthesis pathway. This interference compromises the integrity and functionality of the cell membranes of S. suis . Emodin also triggers the dissipation of the proton motive force, accelerates the tricarboxylic acid cycle, and enhances cellular respiration, ultimately leading to S. suis cell death. Conclusion : This study suggested that emodin inhibits the growth of S. suis via targeting FabF and the inhibition of fatty acid biosynthesis through enzyme-targeted drug design. This represents a novel strategy for developing antimicrobial agents against S. suis and addressing the challenge of antibiotic resistance.
研究领域:
微生物学
·
药理学
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PubMed
高影响因子
危险品化学品经营许可证（带存储）