ANALYTICA CHIMICA ACTA
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2025
·
IF 6
Wenbo Guo,Qingyi Liu,Junhua Yang,Haijuan Zeng,Juan Liu,Lemei Zhu,Dongxia Nie,Zheng Han,Zhihui Zhao
Fluorescent material-based lateral flow immunochromatographic assay (LFIA) has been widespread applied for the point-of-care test of mycotoxins. However, aggregation-caused quenching (ACQ) phenomenon of fluorescent labels seriously affects the detection performance of the methods. Herein, a red-emitted aggregation-induced emission fluorescent microspheres (AIEFMs) based LFIA was developed and firstly applied for the visual and quantitative detection of aflatoxin M1 (AFM1) in milk. The fluorescent probe was constructed by directly coupling the carboxylated AIEPMs with anti -AFM1-mAb, which demonstrated a strong AFM1-specific affinity and exceptional fluorescent characteristics. Under the optimal conditions, this AIEFMs-LFIA could achieve a rapid detection of AFM1 within 15 min, with a visual limit of detection (vLOD) of 0.1 ng/mL and a quantitative limit of detection (qLOD) of 0.01 ng/mL. The accuracy and precision of the established AIEFMs-LFIA method were assessed though the spiked milk samples, and the recoveries were in the range of 86.81%-106.37% with coefficients of variation below 15%. Furthermore, the test strip exhibited a wide detection range for AFM1 (0.01-1 ng/mL) and a remarkable stability for 180 days when stored at 4 °C and 25 °C. Importantly, the results for the spiked milk samples were consistent with those of standard UPLC-MS/MS method, with a correlation coefficient of 0.9911. Overall, the newly developed AIEFMs-LFIA demonstrates significant potential for the point-of-care test of AFM1 in milk.
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高影响因子
PHARMACEUTICAL BIOLOGY
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2025
·
IF 4.8
Yong-xiang Huang,Jin-ru Zhang,Shi-hua Fu,Zhe Liu,Hui-jun Zhong,Qing-yang Zhong,Yin-di Luo,Ying-jie Hu,Hai-peng Zhu,Bin Wen,Song Chen
Context Macrophages play a critical role in the pathogenesis of ulcerative colitis (UC). Indirubin (IDR), a natural ligand of the aryl hydrocarbon receptor (AhR), has been shown to ameliorate DSS-induced colitis in our previous study (Liu Z et al.).Objective To investigate whether IDR exerts its protective effects by regulating M1/M2 polarization and inhibiting ferroptosis in macrophages.Materials and Methods Immunohistochemistry staining targeting CD206 and F4/80 was performed to evaluate the effect of IDR on the polarization of M1/M2 macrophages in colitis. Subsequently, the effects of IDR on the M1- or M2-polarization of THP-1-derived macrophages were investigated. Furthermore, the effects of IDR on ferroptosis in the colon tissue of mice and on RSL3-induced ferroptosis in THP-1-derived macrophages were assessed. The results were verified in mouse peritoneal macrophages.Results In addition to reducing the infiltrated macrophages, IDR treatment preserved CD206+ macrophages in DSS-induced colitis. Using cultured THP-1 cells, we demonstrated that IDR inhibited M1 polarization and prompted M2 polarization. Furthermore, we showed that IDR treatment decreased levels of 4-HNE while increasing GPX4 and NRF2 in DSS-induced colitis and THP-1 cells. IDR treatments also reduced cellular reactive oxygen species (ROS) and iron content, and mitigated RSL3-induced ferroptosis in THP-1-derived macrophages. Similarly, IDR augmented M2-polarization and alleviated ferroptosis in peritoneal macrophages.Discussion and Conclusion IDR skews the polarization of macrophages from M1 to M2. Furthermore, it inhibits ferroptosis in both mice and THP-1-derived macrophages. These mechanisms may contribute to the therapeutic effects of IDR in the treatment of UC.
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高影响因子
Journal of Functional Foods
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2021
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IF 4.451
Yaozhong Hu,Jiaxin Gu,Jing Lin,Yi Wang,Feier Yang,Jia Yin,Zhenting Yu,Sihao Wu,Huan Lv,Xuemeng Ji,Shuo Wang
The intervention of EGCG on M1/M2 macrophage polarization was still unclear and should be studied comprehensively. In this context, the intervention of EGCG on macrophage polarization has been investigated to reveal that EGCG promoted M2 polarization of RAW264.7 upon treating with EGCG. A significant inhibitory effect of EGCG on M1 polarization was observed upon stimulating with LPS and IFN-γ. The expression of macrophage phenotype related marker genes (iNOS, COX-2, IL-1β for M1; Arg-1, Ym-1, IL-10 for M2) demonstrated the suppression of M1 polarization and the promotion of M2 polarization in liver, colon, spleen, and brain. Further analysis against peritoneal macrophages verified the increased M2 phenotypes and decreased M1 macrophages, and the similar variation in liver were confirmed by immunohistochemistry (IHC). No significant variation of spleen macrophages was observed with the general macrophages in declined tendency. Bio-distribution of EGCG and its metabolites (EGC, GA) in different organs has been further determined.
研究领域:
免疫学
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药理学
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细胞生物学
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高影响因子
Science of Advanced Materials
·
2022
·Vol. 14
·期 7
·1175-1184
·
IF 1.067
Mei Qing,Shou Diwen,Quan Ying,Cheng Jiemin,Pan Pan,Chen Huiting,Huang Hongli,Li Yongqiang,Xia Yu,Zhou Yongjian
Lipid deposition is a key predisposing factor of nonalcoholic fatty liver disease (NAFLD). FOXO1 is obviously expressed in polarized M1 macrophages and may cause liver cell steatosis. Thus, silencing FOXO1 during M1 macrophage polarization using small interfering RNA (siRNA) technology
may alleviate lipid deposition in liver cells. However, a lack of effective and biocompatible carriers is challenging for such siRNA-delivery to macrophages. To improve this, RGDfC peptide-modified selenium nanoparticles (RGDfC-Se NPs) were fabricated as a siFOXO1 delivery carrier system.
We showed that RGDfC-Se NPs effectively increased siFOXO1 cellular uptake and silenced FOXO1 expression in human peripheral blood monocyte-like macrophages (THP-1 cells). Additionally, RGDfC-Se@siFOXO1 blocked M1 polarization in these cells. Also, FOXO-1-suppressed cell supernatants extenuated
lipid deposition in LO2 liver cells probably by down-regulating the expression of lipid deposition-related fat metabolic enzymes acetyl-CoA carboxylase 1 and fatty acid synthase. Furthermore, our in vivo analyses showed that RGDfC-Se@siFOXO1 attenuated hepatic steatosis by inhibiting
M1 macrophage polarization in mouse liver tissue. Our studies represent a new strategy and clinic treatment target for NAFLD.
研究领域:
药理学
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分子生物学
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纳米技术
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肝病学
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高影响因子
ANALYTICA CHIMICA ACTA
·
2026
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IF 6.1
Xinying Wang,Yujie Chang,Yiyan Zhang,Xuan Yu,Yixuan Zou,Zheqi Liu,Fuchuan Qi,Jingjing Ming
Accurate and rapid determination of aflatoxin M1 (AFM1) in food is crucial for ensuring the safety of the human diet. In view of this, we proposed a proximity-inducible Cas13a activity and hydrogel-assisted paper-based distance sensor for the detection of aflatoxin M1. The single-stranded DNA (ssDNA) and AFM1 aptamer were split into two parts and linked to the terminus of two separate DNA activator strands, respectively. By introducing AFM1, it stimulated these two DNA activator strands to assemble with CRISPR RNA (crRNA) through spatial proximity mechanism between the target and these two DNA activators to activate the Cas13a trans-cleavage towards the RNA-containing site within hairpin probe to release a DNA initiator. The released DNA initiator triggered the catalytic hairpin assembly (CHA) between magnetic beads (MBs)-DNA capture probe and trypsin-DNA detection probe. After hydrolysis of gelatin hydrogel by trypsin, water released from the hydrogel flowed along the pH indicator strip and exhibited a distinct mark. Depending on this portable method, the limit of detection (LOD) was achieved at 23.6 ng L -1 . Furthermore, our developed strategy can be applied to measure AFM1 in ultra-high temperature (UHT) milk with satisfactory effects, and its excellent specificity and reproducibility also demonstrate that our platform has great potential for application in environmental monitoring.
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高影响因子
IMMUNOLOGY LETTERS
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2023
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IF 4.4
Xiaohui Xia,Zhao Yang,Jiangwei Zhang,Xiongjie Fu,Bin Han,Qijiang Xiong,Anyong Yu
Background Intracerebral hemorrhage (ICH) is a serious medical problem, and promising strategy is limited. Macrophage initiated brain inflammatory injury following ICH, but the molecular mechanism had not been well identified. E3 ligase Nedd4L is implicated in the pathogenesis of the inflammatory immune response. Methods In the present study, we detected the levels of Nedd4L in macrophages following ICH. Furthermore, Macrophage M1 polarization, pro-inflammatory cytokine production, BBB disruption, brain water content and neurological function were examined in ICH mice. Results Here, we demonstrated that E3 ligase Nedd4L levels of macrophage increased following ICH, promoted M1 polarization inflammation by TRAF3. Nedd4L promoted BBB disruption, as well as neurological deficits. Inhibition of Nedd4L significantly attenuated M1 polarization in vivo. Inhibition of Nedd4L decreased TRAF3 and TBK1 levels, and subsequent phosphorylation of p38 and NF-κB p65 subunit following ICH. Conclusions Our data demonstrated that Nedd4L was involved in the pathogenesis of ICH, which promoted inflammatory responses and exacerbated brain damage by TRAF3 following ICH.
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高影响因子
Applied Materials Today
·
2024
·
IF 7.2
Huahui Zeng,Man Li,Zhirong Wang,Tianqi Wang,Zhenqiang Zhang,Xiangxiang Wu
M1 macrophages play a crucial role in the development of rheumatoid arthritis (RA), which can produce various inflammation cytokines, and reactive oxygen species (ROS). Disulfide bonds as reduction-responsive linkages have been extensively employed in the drug delivery systems. However, disulfide bonds are rarely reported in the development of the oxidation-responsive drug carriers. Herein, we designed and synthetized novel oxidation-responsive drug carriers based on disulfide bonds, and further developed nanoparticles (FA-TP@NPs) by self-assembly for the RA treatment. FA-TP@NPs was decorated with folic acid and loaded with triptolide (TP), a potent anti-inflammation Chinese medicine, to target and enter M1 macrophages through the folate receptor on the cytomembrane for simultaneous repolarization of the M2 macrophage and elimination of the M1 macrophage. As expected, FA-TP@NPs exhibited an oxidation-responsive TP release via disulfide-bond oxidation and ester-bond hydrolysis in the presence of intracellular ROS, which accumulated preferentially in inflamed joints. FA-TP@NPs exerted a potent anti-arthritic effect with high biosafety in CIA mice, as evidenced by repolarizing M2 macrophages, inducing M1 macrophage apoptosis, and reducing TNF-α, IL-6, and IL-1β expression. This work shows that FA-TP@NPs give a deep insight into disulfide bond-based oxidation-responsive drug delivery systems, and provide a potential platform for RA treatment.
研究领域:
药学
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免疫学
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纳米医学
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高影响因子
CARBOHYDRATE POLYMERS
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2026
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IF 12.5
Jingya Ruan,Ping Zhang,Jiaming Cheng,Lequan Yu,Yijin Wu,Yinuo Zheng,Yi Zhang,Tao Wang
Two glycans, ZJPr2–2-1 and ZJPr3–2-1 , were isolated from jujube fruits. Structural analysis revealed ZJPr2–2-1 (7.20 kDa) as a previously unreported pectin featuring main chain of →4)- α -D-Gal p A-(1→, →3,4)- α -D-Gal p A-(1→, and →3)- α -L-Rha p -(1→, with side chains containing →4)- α -L-Ara p -(1→, and t-4-deoxy-L- threo -hex-4-enopyranuronic acid (t- α -L-HexA), as well as two isolated fragments linked to →4)- β -D-Gal p A, →4)- α -D-Gal p A. Nevertheless, the absence of HMBC correlations precluded the structural elucidation of its connected side chain. Meanwhile, ZJPr3–2-1 was identified as the first plant-derived cyclic α -1,6-glucan heptasaccharide. Both glycans were found to promote M1 macrophage polarization (increased CD86 and decreased CD206 expression), and enhance the production of pro-inflammatory mediators (NO, iNOS, and TNF- α ) in RAW264.7 cells. The mechanism was supposed to associated with the direct ( ZJPr3–2-1 ) and indirect ( ZJPr2–2-1 ) activation of the Dectin-1/Syk signaling pathway.
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高影响因子
FOOD CHEMISTRY
·
2025
·
IF 9.8
Jun-Qi Song,Qiu-Yi Peng,Mei-Ling Lu,Shu-Zhen Gao,Wen-Bin Liang,Shaoguang Sun,Ruo Yuan,Dong-Rong Xiao
Developing new high-performance electrochemiluminescence (ECL) emitters is a continuous hotspot. Herein, a novel AgNP-decorated porous organic polymer (AgNPs@ETTBC-BPyDAN-POP, BPyDAN = 2,2′-([2,2′-bipyridine]-5,5′-diyl)diacetonitrile) nanocomposite with coreaction accelerator amplification and covalent rigidification-enhanced ECL was prepared. AgNPs@ETTBC-BPyDAN-POP nanocomposite exhibited excellent ECL performance, not only because abundant AIE-active 4′,4″′,4″″′,4″″″′-(ethene-1,1,2,2-tetrayl)tetrakis(([1,1′-biphenyl]-4-carbaldehyde)) (ETTBC) luminogens were covalently assembled and rigidified into ETTBC-BPyDAN-POP network, which diminished radiationless transition, but also because AgNPs functioned as coreaction accelerators that expedited the generation of coreactant radicals, which in-situ react with adjacent ETTBC + intermediates, thereby producing more ETTBC ⁎ excited states for significantly enhancing the ECL emission. Considering the eminent ECL performance, AgNPs@ETTBC-BPyDAN-POP was employed as an ECL indicator to fabricate a supersensitive biosensor for detecting aflatoxin M1, showing a wide response range (5 fg/mL − 500 ng/mL) with a detection limit of 0.57 fg/mL. Overall, this study offered a promising dual-enhancement strategy to boost AIEgens' ECL emission, thereby providing significant inspiration to develop high-efficiency AIEgen-based ECL materials for fabricating hypersensitive ECL biosensors.
研究领域:
材料科学
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分析化学
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纳米技术
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生物传感器
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食品安全
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电化学
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PubMed
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CELLULAR SIGNALLING
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2023
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IF 4.8
Yunyun Li,Ruizhe Li,Hui Qin,Hongliu He,Shanshan Li
Ovarian tumor domain, ubiquitin aldehyde binding 1 (OTUB1), a deubiquitinating enzyme known to regulate the stability of downstream proteins, has been reported to regulate various cancers tumorigenesis, yet its direct effects on oral squamous cell carcinoma (OSCC) progression are unclear. Bioinformatics analysis was performed to screen for genes of interest, and in vitro and in vivo studies were carried out to investigate the function and mechanism of OTUB1 in OSCC. We found that OTUB1 was abnormally elevated in OSCC tissues and positively associated with the pathological stage and tumor stage. Knockdown of OTUB1 impaired the malignance of OSCC cells - suppressed cell proliferation, invasion, migration, and xenografted tumor growth. OTUB1 silencing also drove tumor-associated macrophage M1 polarization but suppressed M2 polarization, and the induction of M1 polarization inhibited the survival of OSCC cells. However, OTUB1 overexpression exerted the opposite effects. Furthermore, the protein network that interacted with the OTUB1 protein was constructed based on the GeneMANIA website. Receptor for activated C kinase 1 (RACK1), a facilitator of OSCC progression, was identified as a potential target of the OTUB1 protein. We revealed that OTUB1 positively regulated RACK1 expression and inhibited RACK1 ubiquitination. Additionally, RACK1 upregulation reversed the effects of OTUB1 knockdown on OSCC progression. Overall, we demonstrated that OTUB1 might regulate OSCC progression by maintaining the stability of the RACK1 protein. These findings highlight the potential roles of the OTUB1/RACK1 axis as a potential therapeutic target in OSCC.
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MOLECULAR AND CELLULAR ENDOCRINOLOGY
·
2023
·
IF 4.1
Xijie Zhou,Chenhao Ye,Liangfu Jiang,Xuwei Zhu,Feiya Zhou,Meizi Xia,Yiheng Chen
A diabetic wound is a refractory disease that afflicts patients globally. MicroRNA-146a-5p (miR-146a-5p) is reported to represent a potential therapeutic target for diabetic wounds. However, microRNA easily degrades in the wound microenvironment. This study extracted bone marrow mesenchymal stem cell (BMSC)-derived exosomes (EXO). Electroporation technology was used to load miR-146a-5p into EXO (labeled as EXO-miR-146a). The endothelial cells (human umbilical vein endothelial cells [HUVECs]) and macrophages were cocultured in transwell chambers in the presence of high glucose. Cell proliferation, migration, and angiogenesis were measured with cell counting kit 8, scratch, and tube forming assays, respectively. Flow cytometry was introduced to validate the biomarker of macrophages and BMSCs. The expression level of macrophage polarization-related proteins and tumor necrosis factor receptor-associated factor 6 (TRAF6) was assessed with western blotting analysis. The full-thickness skin wound model was developed to verify the in vitro results. EXO-miR-146a promoted the proliferation, migration, and angiogenesis of HUVECs in the hyperglycemic state by suppressing the TRAF6 expression in vitro . Additionally, EXO-miR-146a treatment facilitated M2 but inhibited M1 macrophage polarization. Furthermore, EXO-miR-146a enhances reepithelialization, angiogenesis, and M2 macrophage polarization, thereby accelerating diabetic wound healing in vivo . The EXO-miR-146a facilitated M2 macrophage polarization, proliferation, migration, and angiogenesis of HUVECs through TRAF6, thereby ameliorating intractable diabetic wound healing. These results established the basis for using EXO to deliver drugs and revealed mediators for diabetic wound treatment.
研究领域:
干细胞生物学
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分子生物学
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糖尿病研究
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伤口愈合
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免疫学
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高影响因子
International Journal of Nanomedicine
·
2024
·
IF 6.6
Kai Dong,Ying Zhang,Hong Rui Ji,Ze Lin Guan,Dan Yang Wang,Zi Yang Guo,Shu Jing Deng,Bin Yang He,Jian Feng Xing,Cui Yu You
Background The M1/M2 polarization of intestinal macrophages exerts an essential function in the pathogenesis of ulcerative colitis (UC), which can be adjusted to alleviate the UC symptoms.Purpose A kind of pH-sensitive lipid calcium phosphate core-shell nanoparticles (NPs), co-loading with dexamethasone (Dex) and its water-soluble salts, dexamethasone sodium phosphate (Dsp), was constructed to comprehensively regulate macrophages in different states towards the M2 phenotype to promote anti-inflammatory effects.Methods Dex and Dsp were loaded in the outer lipid shell and inner lipid calcium phosphate (Cap) core of the LdCaPd NPs, respectively. Then, the morphology of NPs and methods for determining drug concentration were investigated, followed by in vitro protein adsorption, stability, and release tests. Cell experiments evaluated the cytotoxicity, cellular uptake, and macrophage polarization induction ability of NPs. The in vivo distribution and anti-inflammatory effect of NPs were evaluated through a 2,4,6-trinitrobenzene sulfonic acid (TNBS)-induced BALB/c mice ulcerative colitis model.Results The LdCaPd NPs showed a particle size of about 200 nm and achieved considerable loading amounts of Dex and Dsp. The in vitro and in vivo studies revealed that in the acidic UC microenvironment, the cationic lipid shell of LdCaPd underwent protonated dissociation to release Dex first for creating a microenvironment conducive to M2 polarization. Then, the exposed CaP core was further engulfed by M1 macrophages to release Dsp to restrict the pro-inflammatory cytokines production by inhibiting the activation and function of the nuclear factor kappa-B (NF-κB) through activating the GC receptor and the NF kappa B inhibitor α (I-κBα), respectively, ultimately reversing the M1 polarization to promote the anti-inflammatory therapy.Conclusion The LdCaPd NPs accomplished the sequential release of Dex and Dsp to the UC site and the inflammatory M1 macrophages at this site, promoting the regulation of macrophage polarization to accelerate the remission of UC symptoms.
研究领域:
药学
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免疫学
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消化病学
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PubMed
高影响因子
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