BIOSENSORS & BIOELECTRONICS
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2017
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IF 7.78
Zhiyong Tang,Junlin He,Jun Chen,Yazhen Niu,Yilin Zhao,Yuchan Zhang,Chao Yu
We are presenting an electrochemical immunosensor for the determination of Galectin-3 (Gal-3), a biomarker of heart failure. A glassy carbon electrode (GCE) was modified with a film of a composite made from the N-doped graphene nanoribbons immobilized Fe-based-Metal-organic frameworks deposited with Au nanoparticles (N-GNRs-Fe-MOFs@AuNPs). Primary antibody against Gal-3 (Gal-3-Ab 1 ) was immobilized on the Au nanoparticles on the surface of the modified GCE which then was blocked with bovine serum albumin . Signal amplification is crucial for obtaining low detection limits in biosensors. Here, a relatively simple and ultrasensitive sandwich-type electrochemical immunosensor based on novel signal generation and amplification was developed for the determination of Gal-3. A kind of novel redox-active species, AuPt-Methylene blue (MB) (AuPt-MB) nanocomposites , was synthesized by a one-pot method for the first time. Wherein, MB as a kind of the electron transfer mediators in an amperometric biosensor is responsible for electron production and signal amplification. The rod-like AuPt-MB nanohybrids displayed uniform morphology and good electrochemical activity and can combine with the second antibodies against Gal-3 (Gal-3-Ab 2 ). And the AuPt-MB-Ab 2 coupled with the N-GNRs-Fe-MOFs@AuNPs-Ab 1 to form the sandwich type format that can greatly enhance the biosensor's sensitivity. Under optimal conditions, the designed immunosensor exhibited a linear concentration range from 100 fg mL −1 to 50 ng mL −1 , with a low detection limit of 33.33 fg mL −1 (S/N = 3) for Gal-3 in spiked serum. Additionally, the designed immunosensor showed acceptable selectivity, reproducibility and stability. The satisfactory results in analyzing human serum samples indicated potential application promising in monitoring biomarkers.
研究领域:
生物医学工程
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分析化学
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纳米技术
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PubMed
高影响因子
Nature Communications
·
2026
·
IF 18.1
Zhao Zihan,He Zhen,Gu Hongming,Zhou Andong,Wang Yibing,Liang Zhaoyi,Geng Jie,Xu Xuejiao,Wang Menghui,Li Chunyao,Fan Yuying,Cheng Hairong,Sun Lin,Mayo Kevin H.,Raz Avraham,Tai Guihua,Zhou Yifa
The mechanism of unconventional protein secretion remains an unresolved issue. Here, we describe an unconventional protein secretion pathway for galectin-3 that is mediated by phase separation and condensation. Using four lysosomal damage models, we observed a rapid, pronounced release of galectin-3 in large, non-exosomal particles. This secretion is driven by glycoprotein-induced galectin-3 phase separation and is independent of pyroptosis and secretory autophagy. During phase separation, the S-face of galectin-3 carbohydrate recognition domain binds glycoproteins that triggers galectin-3 N-terminal tail release and condensation. These condensates then recruit ALG-2 via the exposed N-terminal tail. ALG-2 directs the condensates to the endoplasmic reticulum–late endosome interface. After translocation into late endosomes, galectin-3 condensates are secreted into the extracellular milieu by SNARE-dependent vesicular transport. This mechanism of exporting phase-separated protein condensates may serve as a clean-up response to membrane damage.
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高影响因子
INTERNATIONAL JOURNAL OF BIOLOGICAL MACROMOLECULES
·
2025
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IF 8.5
Mingwang Ren,Guoqing Sun,Xiaoyu Ding,Xiaolin Yu,Li He,Shiji Xiao,Minjian Dong,Jianwen Yang,Kan Ding,Chengxin Sun
Polysaccharides are among the key bioactive components of Gynostemma pentaphyllum (Thunb.) Makino . In this study, a novel polysaccharide fraction, GPPA1-1, was isolated from G. pentaphyllum and purified using DEAE-Sepharose Fast Flow, Sephadex G-75, and Sepharose CL-6B column chromatography. GPPA1-1 was determined to have a molecular weight of 3.7 × 10 4 Da and was composed of mannose (Man), glucuronic acid (GlcA), rhamnose (Rha), glucose (Glc), galactose (Gal), and arabinose (Ara) in a molar ratio of 3.88:3.97:21.77:7.02:45.65:17.71. Comprehensive structural characterization was conducted using Congo red staining, FT-IR spectroscopy, Methylation analysis, and NMR analysis. The backbone of GPPA1-1 was identified as comprising →4)-α-Gal p- (1→, →4)-α-Gal p- (3,1→, →2)-α-Rha p- (4,1→, and →2)-α-Rha p- (1→, with branch chains containing α-Ara f -(1→, →5)-α-Ara f -(1→, →3)-α-Galp-(1→, and -α-GlcA-(1→. Biological assays demonstrated that GPPA1-1 effectively alleviates insulin resistance by inhibiting Galectin-3. This activity was confirmed through various experiments, including Galectin-3-mediated hemagglutination, Western blotting, CETSA, and glucose uptake assays. These findings highlight the potential of GPPA1-1 as a promising therapeutic agent for managing insulin resistance.
研究领域:
植物化学
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代谢生物学
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药理学
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PubMed
高影响因子
CARBOHYDRATE POLYMERS
·
2025
·
IF 12.5
Yuanyuan Chen,Qian Zhou,Yue Zhou,Jinlan Huang,Renjie Niu,Jian Ming,Mingfu Wang
Oral delivery of natural antioxidants represents a promising therapeutic strategy for ulcerative colitis (UC), yet their therapeutic efficacy is hindered by instability and poor accumulation at inflamed sites. To address this, we developed Galectin-3 (Gal-3)-targeted nanoparticles (ZDP-NPs) by encapsulating diosmetin within zein complexes modified with a galactose- and rhamnogalacturonan-I (RG-I)-rich pectin (PMTP, Mw: 228.8 kDa, DM: 34.21 %, RG-I content: 43 %) extracted from Premna microphylla Turcz leaves. Surface plasmon resonance (SPR) analysis confirmed a strong binding affinity between PMTP and Gal-3 (KD = 2.83 μM). ZDP-NPs exhibited uniform spherical morphology (~170 nm), high drug loading (87.9 %) and colloidal stability. Under simulated gastrointestinal conditions, ZDP-NPs showed reduced Dio release (45.6 %) compared to PMTP-free nanoparticles (ZD-NPs, 75.6 %). In vitro studies showed that PMTP surface modification significantly enhanced nanoparticle uptake by LPS-induced macrophages via Gal-3-mediated endocytosis. In vivo colitis experiment of mice revealed that ZDP-NPs selectively accumulated in inflamed colons via Gal-3 targeting, prolonged retention, and significantly alleviated colonic damage by reducing oxidative stress, suppressing pro-inflammatory cytokines, and restoring epithelial barrier integrity. Biocompatibility assays confirmed minimal toxicity of ZDP-NPs. This study presented a food-derived pectin-based nanoplatform for precise colitis intervention through Gal-3 targeting, offering a multifaceted strategy to break the inflammation-oxidative stress cycle.
研究领域:
纳米医学
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药理学
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胃肠病学
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生物化学
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炎症性肠病研究
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植物来源药物
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高影响因子
Chinese Journal of Natural Medicines
·
2026
·Vol. 24
·期 2
·227-236
·
IF 7.5
Rakotomalala Manda Heriniaina,Xia Chen,Yulian Wu,Wenfeng Liao,He Fei,Peipei Wang,Kan Ding
Pancreatic cancer, specifically pancreatic ductal adenocarcinoma (PDAC), ranks among the most prevalent malignancies and is a leading cause of cancer-related mortality worldwide. Therefore, there is an urgent need to identify novel anti-pancreatic cancer agents. This study reports a newly identified homogeneous polysaccharide, designated ESPPW, isolated from Arthrospira platensis ( A. platensis ). The molecular weight of ESPPW is estimated at 356 kDa, and it consists predominantly of glucose and rhamnose, with minor amounts of mannose, glucuronic acid, galacturonic acid, galactose, xylose, arabinose, and fucose. ESPPW inhibits the proliferation and migration of PDAC cells both in vitro and in vivo . Mechanistic investigations reveal that ESPPW induces apoptosis through activation of caspase-3 and is associated with upregulation of the tumor-suppressor protein p53. Notably, treatment with 2.8 nmol·L −1 of ESPPW leads to significant time-dependent downregulation of galectin-3 (Gal-3) and glypican-6 (GPC-6). These findings are corroborated by immunohistochemical analysis of tumor xenograft tissues. Furthermore, overexpression of Gal-3 and GPC-6 reverses the pro-apoptotic effect of ESPPW, as indicated by restored cycle regulatory proteins (CDK2) expression. In conclusion, these data demonstrate that ESPPW suppresses PDAC cell growth by promoting apoptosis and disrupting the functional activity of Gal-3 and GPC-6.
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CARBOHYDRATE POLYMERS
·
2021
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IF 9.381
Xianglin Pan,Haoyu Wang,Ziming Zheng,Xiao Huang,Linlin Yang,Junxi Liu,Kaiping Wang,Yu Zhang
Ulcerative colitis (UC) is an inflammatory bowel disease that affects the colon and rectum. Although galectin-3 (Gal-3) has been reported to play a proinflammatory role in UC, it is unknown whether pectic polysaccharide , a Gal-3 inhibitor in tumor metastasis, can alleviate UC by inhibiting Gal-3. The aim of this study was to investigate the anti-inflammatory effects and underlying mechanisms of SCLP, a pectic polysaccharide purified from Smilax china L. in our previous work, on dextran sulfate sodium-induced UC in BALB/c mice. The results showed that SCLP could significantly improve symptoms, alleviate histopathological damage and reduce the secretion of inflammatory mediators in mice with UC. Analysis of the anti-colitis mechanisms indicated that SCLP could inhibit the Gal-3/NLRP3 inflammasome/IL-1β pathway by suppressing the expression of Gal-3 and the interaction of Gal-3 and NLRP3 . Our results suggested that SCLP could be a promising candidate for prevention and treatment of UC.
研究领域:
药理学
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炎症性肠病
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免疫学
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胃肠病学
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高影响因子
Marine Drugs
·
2025
·Vol. 23
·期 11
·423
·
IF 5.4
Pingting Liu,Fengyuan Li,Zhicong Liu,Yang Liu
Galectin-3 (Gal-3) is a histologic marker of pancreatic cancer and a potential therapeutic target. This study aimed to characterize a novel sulfated agarose-derived oligosaccharide (DP9) from marine algae,Gracilaria lemaneiformis, evaluate its Gal-3 inhibitory activity, and investigate its anti-pancreatic cancer mechanisms. Through controlled acid hydrolysis, a series of odd-numbered oligosaccharides (DP3-11) were obtained, in which DP9 showed the strongest Gal-3 inhibition in hemagglutination assays. Structural analysis confirmed DP9’s unique composition including an alternating β (1→4)-D-galactose and α (1→3)-3,6-anhydro-L-galactose backbone, featuring partial 6-O-methylation on β-D-galactose and 6-O-sulfation on 3,6-anhydro-α-L-galactose residues. Molecular docking revealed DP9’s binding to Gal-3’s carbohydrate recognition domain through key hydrogen bonds (His158, Arg162, Lys176, Asn179 and Arg186) and hydrophobic interactions (Pro117, Asn119, Trp181 and Gly235), with the sulfate group enhancing binding affinity. In vitro studies demonstrated DP9’s selective anti-pancreatic cancer activity against BxPC-3 cells, including inhibition of cell proliferation; S-phase cell cycle arrest; induction of apoptosis; and suppression of migration and invasion. Mechanistically, DP9 attenuated the Gal-3/EGFR/AKT/FOXO3 signaling pathway while showing minimal cytotoxicity to normal cells. This study first demonstrated that agarose-derived odd-numbered oligosaccharides (DP9) can serve as effective Gal-3 inhibitors, which proved its potential as a marine oligosaccharide-based therapeutic agent for pancreatic cancer.
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高影响因子
Nature Communications
·
2025
·Vol. 16
·期 1
·1-23
·
IF 15.7
Zhang Zhongyu,Zhao Zhengde,Huang Xiuyi,Zhou Lifang,Jiang Xin,Wu Haoliang,Liu Chenshu,Huang Kan,Wen Jielu,Liu Yunchong,Miller Michelle C.,Zhao Zihan,He Zhen,Wang Yuxin,Liu Siyu,Huang Lijin,Yuan Lining,Zeng Renli,Cen Zhipeng,Chen Anning,Chen Yanbo,Zeng Gang,Liu Wenzhou,Hong Xiaosi,Ren Meng,Yan Li,Zhang Yang,Guan Dongxian,Tian Xiaoyu,Cai Weikang,Tai Guihua,Mayo Kevin H.,Zhou Yifa,Li Zilun,Chen Sifan
Diabetic foot ulcers are severe diabetic complications, and promoting impaired angiogenesis is essential for wound healing. Pro-angiogenic galectin-3 is elevated in diabetic serum and promotes systemic insulin resistance that may impair wound healing. However, the exact role of galectin-3 in the regulation of diabetic wound healing remains unclear. Here, we demonstrate that galectin-3 promotes skin wound healing and angiogenesis via binding to its receptor integrin α5β1, and enhances downstream focal adhesion kinase phosphorylation by forming a liquid-liquid phase separation with integrin α5β1. Under diabetic conditions, aberrant accumulated advanced glycation end-products bind to galectin-3, blocking its interaction with integrin α5β1 and impairing angiogenesis. Topical treatment of recombinant galectin-3 in hydrogels promotes diabetic wound healing in rodents without causing systemic insulin resistance and synergizes with insulin. This study clarifies the binding of galectin-3 to integrin α5β1, instead of advanced glycation end-products, forming phase separation to promote angiogenesis and diabetic wound healing, laying the foundation for local galectin-3 therapy to treat diabetic foot ulcers.
研究领域:
糖尿病研究
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细胞生物学
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分子生物学
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伤口愈合
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血管生成
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糖生物学
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药理学
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INTERNATIONAL JOURNAL OF PHARMACEUTICS
·
2020
·
IF 4.845
Xia Yuan,Li Liu,Wei Wang,Ya-ru Gao,Die Zhang,Ting-ting Jia,Hai-rong Zeng,Gang Pan,Yi Yuan
The development of small molecule anticancer drugs , with low water solubility and high toxicity, into polymeric prodrugs has developed into a promising strategy in clinical application. In this study, we synthesized a novel G3-C12-mediated esterase-sensitive tumor-targeting polymeric prodrug of camptothecin (CPT), P(OEGMA- co -CPT- co -G3-C12), and explored its anticancer activity against androgen-independent prostate cancer in vitro and in vivo. Compared to free CPT, the multifunctional polymeric prodrug demonstrated improved water solubility and stability, higher intracellular uptake, and enhanced cytotoxicity in DU145 cells in vitro. Furthermore, it displayed an improved accumulation in the tumor and an enhanced anticancer activity in vivo. Hence, P(OEGMA- co -CPT- co -G3-C12) could be a promising drug in the treatment of androgen-independent prostate cancer.
研究领域:
肿瘤学
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药学
·
癌症治疗
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PubMed
高影响因子
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
·
2026
·
IF 2.5
Chunhui Shan,Qi Bing,Gang Qiu,Hui Zhang,Yingmin Chen
Galectin-3 disrupts microglial P2X7R/MerTK balance after stroke • ERK/ROS/BRD4 axis mediates Gal-3-induced P2X7R upregulation • Gal-3 promotes cGAS-STING inflammation and apoptosis via HIF1α/P2X7R • TD-139 restores P2X7R/MerTK balance and reduces cerebral infarction • Targeting Gal-3 improves motor, cognitive, and grip strength in MCAO rats This study demonstrates that Galectin-3 (Gal3) exacerbates cerebral infarction progression by modulating the P2X7R/MerTK equilibrium in microglia via the ERK/BRD4/HIF1α signaling axis, with reactive oxygen species (ROS) serving as a potential intermediate mediator linking ERK activation to BRD4 upregulation based on prior literature evidence. Single-cell transcriptomic analysis revealed that ischemia drives microglia from a homeostatic state to an activated disease phenotype, and virtual Gal3 knockout predicted corresponding downregulation of BRD4. Using a rat model of cerebral infarction, we found that the Gal3 inhibitor TD-139 significantly reduced infarct volume, promoted M2 polarization of microglia, and improved neurological function in behavioral assays. Mechanistic investigations in BV2 microglia revealed that Gal3 activates ERK1/2, leading to ROS accumulation, BRD4 upregulation, and subsequent HIF1α-mediated P2X7R transcription, while suppressing KLF4 and MerTK. This cascade increased P2X7R expression and suppressed MerTK/KLF4 expression, generating a pro-inflammatory and pro-apoptotic microenvironment. Notably, pharmacological inhibition of Gal3 enhanced efferocytosis and reduced apoptosis, whereas P2X7R blockade exerted similar neuroprotective effects. These findings identify Gal3 as a key regulator of microglial polarization via the experimentally validated ERK/BRD4/HIF1α-P2X7R signaling cascade, where P2X7R activation concurrently triggers cGAS-STING-mediated pro-inflammatory/pyroptotic responses and suppresses the KLF4/MerTK efferocytosis axis. Targeting this regulatory network could provide therapeutic benefits in cerebral infarction by shifting microglia toward the neuroprotective M2 phenotype and facilitating inflammation resolution. Targeting this pathway could provide therapeutic benefits in cerebral infarction by shifting microglia toward the neuroprotective M2 phenotype and facilitating inflammation resolution. Data were analysed using one-way ANOVA followed by Tukey's post-hoc test for multiple comparisons; P < 0.05 was considered statistically significant.
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高影响因子
CARBOHYDRATE POLYMERS
·
2020
·
IF 7.182
Dongmei Wu,Jiaqi Zheng,Weiwei Hu,Xiaoliang Zheng,Qiaojun He,Robert J. Linhardt,Xingqian Ye,Shiguo Chen
Rhamnogalacturonan I (RG-I) pectin are regarded as strong galectin-3 (Gal-3) antagonist because of galactan sidechains. The present study focused on discussing the effects of more structural regions in pectin on the anti-Gal-3 activity. The water-soluble pectin (WSP) recovered from citrus canning processing water was categorized as RG-I pectin. The controlled enzymatic hydrolysis was employed to sequentially remove the α-1,5-arabinan, homogalaturonan and β-1,4-galactan in WSP. The Gal-3-binding affinity KD (kd/ka) of WSP and debranched pectins were calculated to be 0.32 μM, 0.48 μM, 0.56 μM and 1.93 μM. Moreover, based on the more sensitive cell line (MCF-7) model, the IC 30 value of WSP was lower than these of modified pectins, indicating decreased anti-Gal-3 activity. Our results suggested that the total amount of neutral sugar sidechains, the length of arabinan and cooperation between HG and RG-I played important roles in the anti-Gal-3 activity of WSP, not the Gal/Ara ratio or RG-I/HG ratio. These results provided a new insight into structure-activity relationship of citrus segment membrane RG-I as a galectin-3 antagonist and a new functional food.
研究领域:
食品科学
·
分子生物学
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PubMed
高影响因子
INFLAMMATION
·
2026
·
IF 5.4
Ren Niansheng,Li Ruixi,Tao Qiang,Hong Shengjie,Wang Jicai,Zha Jiandong,Wang Shikai,Zhang Guangquan
Chronic pancreatitis (CP) is a chronic disease characterized by pancreatic fibrosis driven by pancreatic stellate cell activation and M2 polarization of macrophages. Nicotinamide n-methyltransferase (NNMT) is a methylase critically involved in fibrosis. Galectin-3 (LGALS3), a member of the galectin family, drives M2 macrophage polarization. This study explores the roles of NNMT and LGALS3 in CP. CP was induced in C57BL/6 mice via repeated intraperitoneal injections of 50 µg/kg cerulein. NNMT was upregulated in pancreatic tissues of CP mice, especially in mouse pancreatic stellate cells (mPSCs). Functional inhibition of NNMT in mPSCs, via lentiviral short-hairpin RNA-mediated knockdown or treatment with NNMT inhibitor, suppressed mPSC activation, proliferation, and migration. Moreover, conditioned medium from mPSCs with NNMT inhibition reduced M2 polarization of bone marrow-derived macrophages (BMDMs). In vivo, intraperitoneal administration of 20 mg/kg NNMT inhibitor for 28 days alleviated pancreatic collagen deposition and macrophage M2 polarization, resulting in reduced pancreatic fibrosis. RNA sequencing and bioinformatics analysis identified LGALS3 as a potential downstream target of NNMT. NNMT inhibition downregulated LGALS3 expression in mPSCs, and chromatin immunoprecipitation - quantitative polymerase chain reaction (ChIP-qPCR) confirmed that this suppression was associated with increased trimethylation of lysine 27 on histone H3 (H3K27me3) enrichment at the LGALS3 promoter. Lentivirus-mediated LGALS3 overexpression reversed the inhibitory effect of NNMT knockdown on BMDM M2 polarization. In conclusion, inhibition of NNMT alleviates mPSC activation and suppresses mPSC-induced macrophage M2 polarization via H3K27me3-mediated repression of LGALS3 transcription, with the ultimate effect of mitigating cerulein-induced pancreatic fibrosis.
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