FOOD CONTROL
·
2025
·
IF 6.3
Chanchiang Liang,Siyang Chen,Wenxiu Zhu,Hanzheng Dou,Xiaodong Xia
The antimicrobial efficacy of punicalagin against foodborne pathogens has been extensively studied, yet its impact on spoilage microorganisms remains poorly characterized. This study aimed to evaluate punicalagin's inhibitory effects on Pseudomonas fluorescens and explore its potential application in tilapia preservation. Growth curve analysis showend that punicalagin effetively inhibited the growth of Pseudomonas fluorescens . In addition, punicalagin triggered intracellular potassium ion efflux and leakage of nucleic acids and protein. Scanning electron microscopy revealed compromised cell membrane integrity after punicalagin treatment. Furthermore, punicalagin exposure reduced intracellular ATP levels and elevated reactive oxygen species accumulation. Concurrently, it effectively suppressed biofilm formation and destroyed preformed biofilms. In tilapia spiked with Pseudomonas fluorescens , punicalagin markedly attenuated spoilage progression, as evidenced by diminished protein degradation and lipid oxidation. These collective findings indicate that punicalagin exhibit antimicrobial and anti-biofilm activities against Pseudomonas fluorescens , highlighting its potential as a natural preservative for aquatic products.
研究领域:
食品科学
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微生物学
·
水产品加工
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DOI
高影响因子
JOURNAL OF SEPARATION SCIENCE
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2016
·Vol. 39
·期 10
·1963-1970
·
IF 2.741
Guang-Ying Sun,Chao Wang,Yu-Qin Luo,Yong-Xin Zhao,Jian Yang,Zhao-Sheng Liu,Haji Akber Aisa
The combination of molecular crowding and virtual imprinting was employed to develop a cost-effective method to prepare molecularly imprinted polymers. By using linear polymer polystyrene as a macromolecular crowding agent, an imprinted polymer recognizable to punicalagin had been successfully synthesized with punicalin as the dummy template. The resulting punicalin-imprinted polymer presented a remarkable selectivity to punicalagin with an imprinting factor of 3.17 even at extremely low consumption of the template (template/monomer ratio of 1:782). In contrast, the imprinted polymer synthesized without crowding agent, did not show any imprinting effect at so low template amount. The imprinted polymers made by combination of molecular crowding and virtual imprinting can be utilized for the fast separation of punicalagin from pomegranate husk extract after optimizing the protocol of solid-phase extraction with the recovery of 85.3 ± 1.2%.
研究领域:
分析化学
·
天然产物分离纯化
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DOI
PubMed
高影响因子
Food & Function
·
2024
·
IF 5.1
Huanhuan Liu,Chunhong Yan,Yue Teng,Jian Guo,Chencheng Liang,Xiaodong Xia
Background: Inflammatory bowel disease (IBD) is an increasing health burden worldwide. Punicalagin, a bioactive component rich in pomegranate rind, has been shown to attenuate chemical or bacteria-induced experimental colitis in mice, but whether punicalagin exerts its function through modulating gut microbiota and metabolites remains unexplored. Results: Punicalagin (100 mg per kg per day) administered orally to mice alleviated dextran-sodium sulfate (DSS)-induced colitis. Gut microbiota analyzed by 16S rRNA sequencing showed that punicalagin altered gut microbiota by increasing the Lachnospiraceae_NK4A136_group and Bifidobacterium abundance. To evaluate the effect of punicalagin-modulated microbiota and its metabolites in colitis mice, we transplanted fecal microbiota and sterile fecal filtrate (SFF) to mice treated with oral antibiotics. The results of fecal microbiota transplantation (FMT) demonstrated that punicalagin's anti-colitic effect is transferable by transplanting punicalagin-modulated gut microbiota and its metabolites. Additionally, we discovered that punicalagin-modulated sterile fecal filtrate also exhibits anti-colitis effects, as evidenced by improved intestinal barrier integrity and decreased inflammation. Subsequently, fecal metabolites were analyzed using liquid chromatography-mass spectrometry (LC-MS). The analysis revealed that punicalagin significantly increased the level of D-ribose. In vitro experiments showed that D-ribose has both anti-inflammatory and antioxidant properties. Furthermore, D-ribose significantly mitigated DSS-induced colitis symptoms in mice. Conclusions: Overall, this study demonstrated that gut microbiota and its metabolites partly mediate the protective effect of punicalagin against DSS-induced colitis in mice. D-ribose is a key metabolite that contributes to the anti-colitic effect of punicalagin in mice.
研究领域:
胃肠病学
·
微生物学
·
药理学
·
代谢组学
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DOI
PubMed
高影响因子
Analytical Methods
·
2016
·Vol. 8
·期 23
·4554-4562
·
IF 1.915
Man Jia,Guang-Yin Sun,Yong Xin Zhao,Zhao-Sheng Liu,Haji Akber Aisa
The efforts in the present work focus on the topic of reducing template consumption in the preparation of molecularly imprinted polymers (MIPs). For this purpose, the effect of polyethylene glycol (PEG) as a molecular crowding agent on reducing template consumption in the preparation of MIPs was investigated. To prepare MIP monoliths with punicalagin, acrylamide was used as the functional monomer, and ethylene glycol dimethacrylate was the cross-linking monomer, with a mixture of PEG–THF–toluene as a porogen. It was found that the molecular weight of PEG, the ratio of the template to functional monomer, amount of PEG, level of DMF and the composition of the mobile phase greatly affected the retention of the template and the performance of molecular recognition. The PEG-based imprinted monolith still showed a specific imprinting effect even at the ratio of functional monomer to template of 1353 : 1. The optimal MIPs can be used as solid-phase extraction sorbents for the purification of punicalagin with a recovery of 85% and a purity of 97.7% from the crude extract of pomegranate-rind.
研究领域:
材料科学
·
分析化学
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DOI
高影响因子
BONE
·
2021
·
IF 4.398
FeiFei Liu,Hao Yang,DongZhe Li,XueJian Wu,QiCai Han
Background Punicalagin (PUN) is a common anti-inflammatory polyphenol. However, the function and mechanism of PUN in osteoarthritis remains unknown. Methods Chondrocytes were isolated from rats, and confirmed by toluidine blue staining and immunofluorescence. Chondrocytes were challenged by lipopolysaccharide (LPS), and rat osteoarthritis model was established by Hulth method. The secretion of inflammatory factors, cell viability and apoptosis were tested via enzyme linked immunosorbent assay (ELISA), MTT and flow cytometry. The levels of forkhead box O1 (Foxo1), proteoglycan 4 (Prg4), hypoxia-inducible factor-3α (HIF3α), autophagy-related genes or extracellular matrix (ECM)-related proteins were examined via quantitative reverse transcription polymerase chain reaction (qRT-PCR), western blot or immunohistochemistry . The cartilage tissue damage was assessed via hematoxylin-eosin (HE) staining, toluidine blue staining and terminal dexynucleotidyl transferase (TdT)-mediated dUTP nick and labeling (TUNEL) staining. Results LPS triggered inflammatory injury in chondrocytes. PUN promoted autophagy to mitigate LPS-induced inflammatory injury. Foxo1 silence attenuated the effect of PUN on LPS-mediated autophagy inhibition and inflammatory injury. Promotion of Prg4/HIF3α axis abolished the influence of Foxo1 knockdown on LPS-mediated chondrocytes injury. PUN mitigated the inflammatory injury in rat osteoarthritis model by promoting autophagy and inhibiting inflammation and ECM degradation via Foxo1/Prg4/HIF3α axis. Conclusion PUN attenuates LPS-induced chondrocyte injury and osteoarthritis progression by regulating Foxo1/Prg4/HIF3α axis.
研究领域:
药理学
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风湿病学
·
细胞生物学
·
分子生物学
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DOI
PubMed
高影响因子
FOOD CONTROL
·
2022
·
IF 6.652
Hongli Liu,Wenxiu Zhu,Yu Cao,Jingzhu Gao,Tong Jin,Ningbo Qin,Xiaodong Xia
Vibrio parahaemolyticus is a major food-borne pathogen and the leading cause of seafood-associated enteric infections worldwide. In addition, imprudent use of antibiotics has contributed to increasing antibiotic resistance in V. parahaemolyticus. Therefore, there is an urgent need to develop novel control strategies to reduce V. parahaemolyticus contamination and infection. V. parahaemolyticus could form biofilm on different surfaces and contains several virulence factors, which together contribute to its persistence and pathogenicity. In this study, anti-biofilm and potential anti-virulence effects of punicalagin against V. parahaemolyticus were investigated. Punicalagin at sub-inhibitory concentrations (3.125–12.5 μg/mL) exerted significant anti-biofilm activity (20.9–74.4% reduction). It decreased bacterial motility, and attenuated metabolic activity of cells inside biofilm. Meanwhile, punicalagin inhibited EPS production and caused reduction of exopolysaccharides in biofilms, and decreased Raman peak intensities of different biofilm components. Moreover, punicalagin significantly inhibited V. parahaemolyticus adhesion to Caco-2 cells (23.8–68.1% reduction) and downregulated expression of genes involved in V. parahaemolyticus biofilm formation and virulence. These findings suggest that punicalagin could be potentially developed as an alternative strategy to control V. parahaemolyticus biofilms in food industry and mitigate diseases caused by this pathogen.
研究领域:
微生物学
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食品安全
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药理学
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分子生物学
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DOI
高影响因子
JOURNAL OF CHROMATOGRAPHY A
·
2017
·
IF 3.981
Guangying Sun,Yanfang Liu,Hasanjan Ahat,Aijin Shen,Xinmiao Liang,Xingya Xue,Yuqin Luo,Jian Yang,Zhao-Sheng Liu,Haji Akber Aisa
In this study, “two dimensional” molecularly imprinted solid-phase extraction (2D-MIP-SPE) of semi-preparative grade was constructed to fast purify ellagitannins in pomegranate husk extract with the help of crystallization and reverse-phase liquid chromatgoraphy (RPLC). Ellagic acid and punicalagin imprinted polymers were synthesized in batch mode and two semi-preparative MIP-SPE columns were individually packed. After investigaing “functional complementation”, 2D-MIP-SPE was constructed using ellagic acid MIP and punicalagin MIP-SPE as the first and second dimension, respectively. Then, pomegranate husk extract was fast divided into four fractions individually enriching in ellagic acid, granatin A, punicalagin and ellagic acid glucoside by 2D-MIP-SPE. With the aid of crystallization and RPLC, ellagic acid (13.5 mg) and punicalagin (53.4 mg) were fast obtained in 30 min. Ellagic acid glucoside was purified to the purity near 100% with a recovery of 86.1%. Granatin A (92%) was directly obtained by 2D-MIP-SPE with the recovery of 81.8%. All above indicated that 2D-MIP-SPE was highly efficient in natural product purification. The concept of “functional complementation” was expected to be a useful tool in the construction of 2D-MIP-SPE.
研究领域:
分析化学
·
天然产物化学
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产品关联
DOI
PubMed
高影响因子
IUBMB LIFE
·
2026
·Vol. 78
·期 1
·e70088
·
IF 3.2
Yuan-yuan Fang,Si-yi Zhang,Chuan-yu Leng,Jing-Lv,Shu-fen Zhao,Xue-ying Sun,Xin-Li,Yang-yang Lu,Bing-Wang,Wei-wei Qi
Gastric cancer represents the fifth most common malignancy globally and the third leading cause of cancer-related deaths. Due to its insidious early symptoms and frequent metastasis at diagnosis, the survival rate remains dismal. There is thus an urgent clinical need for novel therapeutic agents. Innovative strategies combining traditional chemotherapy with interventions that induce novel cell death pathways represent a promising translational direction for improving patient outcomes. Punicalagin (PUN), a natural polyphenol derived from pomegranate, exhibits potent antioxidant and broad-spectrum antitumor activities, yet its role in gastric cancer remains understudied. Three gastric cancer cell lines (AGS, HGC27, MFC) and one normal gastric mucosal epithelial cell line (GES-1) were initially selected for in vitro experiments. The effects of PUN on gastric cancer cells and normal gastric mucosal epithelial cells were assessed through MTT assay, propidium iodide (PI) staining, and cell colony formation assays, while cell migration ability was evaluated using a scratch wound healing assay. The inhibitory effect of PUN on gastric cancer was tested in a subcutaneous tumor model in nude mice, with pathological changes in vital tissues and organs observed via hematoxylin and eosin (H&E) staining. Subsequently, transcriptome sequencing was performed, and JC-1, H2DCFDA, and DHE staining methods were employed to measure mitochondrial function and reactive oxygen species (ROS) levels in PUN-treated cells. Western blotting was used to detect the expression of apoptosis- and cell cycle-related proteins. Next, two gastric cancer cell lines (AGS, HGC27) were selected for in vitro experiments to assess the combined effects of PUN and the copper ionophore elesclomol (ES) (hereafter referred to as ES-Cu, representing the combination of ES and Cu 2+ ). Cell viability was assessed using the MTT assay, and morphological changes were observed under a microscope. Cell proliferation and migration abilities were assessed via colony formation and scratch wound healing assays, respectively. Fluorescence staining was used to examine mitochondrial function and ROS levels in cells co-treated with PUN and ES-Cu. Laser confocal microscopy and Western blotting were employed to determine the oligomerization level of DLAT protein by quantifying soluble and insoluble protein expression, along with the expression of ACO2, ETFDH, FDX1, and LIAS proteins. Molecular docking, molecular dynamics simulations, immunofluorescence staining, and transfection techniques were utilized to confirm the critical role of FDX1 in copper-induced cell death following co-treatment with PUN and ES-Cu. We found that PUN could suppress the viability, proliferation, and migration of gastric cancer cells in a concentration- and time-dependent manner. Subsequent in vivo experiments demonstrated that PUN inhibited tumor growth in nude mice at a safe dosage. Besides, transcriptome sequencing and Western blot analysis revealed that PUN induced cell cycle arrest and apoptosis. Secondly, the cell death mechanism triggered by PUN was closely associated with mitochondrial stress. PUN increased intracellular ROS levels and reduced mitochondrial membrane potential. Transcriptome sequencing and proteomic analysis further revealed molecular changes at both the mRNA and protein levels, with differential gene analysis identifying potential targets and pathways. Moreover, when PUN was combined with ES-Cu, cell viability, proliferation, and migration were all suppressed, while exacerbating mitochondrial dysfunction and elevated oxidative stress. Laser confocal microscopy and Western blotting were used to assess the expression of soluble and insoluble proteins, confirming the oligomerization of the DLAT protein. Western blot also showed that PUN could regulate the expression levels of ACO2, ETFDH, FDX1, and LIAS proteins. Molecular docking, molecular dynamics simulations, and siRNA transfection were performed to confirm the critical role of ferredoxin 1 (FDX1) in copper-induced cell death. Furthermore, when used in combination with chemotherapy drugs, PUN exhibited synergistic inhibitory effects on gastric cancer growth. PUN demonstrates significant antitumor activity both in vivo and in vitro by inducing mitochondrial dysfunction, which subsequently triggers apoptosis. In combination therapy strategies, PUN can work synergistically with chemotherapy drugs to suppress gastric cancer growth. Furthermore, PUN enhances its inhibitory effect on gastric cancer by working synergistically with cuproptosis through targeting FDX1.
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DOI
高影响因子
LWT-FOOD SCIENCE AND TECHNOLOGY
·
2022
·
IF 6.056
Zi-Yi Yu,Ke Xu,Xuan Wang,Yi-Ting Wen,Lin-Jun Wang,De-Qiang Huang,Xiao-Xin Chen,Wei-Ming Chai
The inhibition of punicalagin on tyrosinase and melanogenesis was investigated through multiple spectroscopic approaches, molecular docking, molecular dynamic simulation, cell assay, and preservation assays. The results confirmed that punicalagin significantly inhibited tyrosinase activity in vitro (IC 50 = 0.64 ± 0.05 mM) and B16F10 cells (IC 50 = 16 ± 0.7 μM). The binding of punicalagin to tyrosinase changed the conformation of the enzyme by influencing the hydrophobicity and polar environment of the binding site. The results of molecular docking and thermodynamic analysis showed that hydrophobic interaction and hydrogen bond were major driving forces in stabilizing the punicalagin-tyrosinase complex, influencing substrate-binding affinity to tyrosinase and resulting in tyrosinase activity reduction. Molecular dynamic analysis indicated that punicalagin stretched the basic framework structure of tyrosinase and lowered the surface hydrophobicity of the enzyme. Cell analyses further demonstrated that punicalagin inhibited melanogenesis by down-regulating the expressions of MITF and tyrosinase. What's more, preservation assays showed that punicalagin could reducing the oxidation of phenols to melanin by inhibiting the polyphenol oxidase, thereby preventing the browning of fresh-cut apples. These findings provided new perspectives on the inhibition mechanism of punicalagin on tyrosinase/melanogenesis and a theoretical support for its feasible application in the food and medicine industry.
研究领域:
生物化学
·
药理学
·
细胞生物学
·
食品科学
·
医学
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DOI
高影响因子
Foods
·
2019
·Vol. 8
·期 12
·606
·
IF 3.011
Hong Peng,Bin Li,Jing Tian
The study explored punicalagin (PGN) as a wheat flour enhancer. The impact of PGN on the physicochemical and structural properties of wheat flour have been investigated. It turned out that PGN increased the formation time, stability, tensile resistance, extension, and viscoelasticity of the dough at the concentrations of 0.13 and 0.26 mg/g. Scan electron microscope images of the cross section of the dough displayed a more compact and ordered network structure with the addition of 0.13 and 0.26 mg/g PGN. Fourier transform infrared spectroscopy spectra indicated an increase of α-helix and β-sheet content. However, nonlinear enhancing effects of PGN on the stretching properties, rheology, and structural properties of the dough were observed at concentrations of 0.39 and 0.52 mg/g. Correspondingly, cleavages were observed on the cross section of the dough and the content of β-sheet showed a trend of reduction in the dough with addition of PGN at high concentrations. Taken together, these results indicated the potential usage of PGN as a wheat flour enhancer of natural origin at the concentration below 0.39 mg/g in the flour.Keywords:punicalagin;wheat flour;dough rheology;gluten protein network
研究领域:
食品科学
·
植物化学
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DOI
PubMed
高影响因子
INTERNATIONAL DENTAL JOURNAL
·
2026
·Vol. 76
·期 5
·109801
·
IF 5.2
Yumeng Yang,Xin Li,Qianwen Tang,Chengfei Zhang,Zehao Chen,Wei Liu
Aim Punicalagin (PCG), a natural polyphenol derived from pomegranate peel, possesses well-established antibacterial and anti-inflammatory properties. However, whether PCG promotes odontogenic differentiation of human dental pulp stem cells (DPSCs) remains unclear. This study investigated the effects of PCG on odontogenic differentiation and reparative dentin formation and further explored the underlying molecular mechanism. Methods A rat pulpitis model was established to evaluate the effects of a PCG-loaded collagen sponge on pulpal repair. Pulpal inflammation and reparative dentin formation were assessed histologically. DPSCs were isolated and treated with PCG (5 μM). Cell viability, odontogenic differentiation, and Wnt/β-catenin signalling were evaluated using CCK-8, alkaline phosphatase (ALP) and Alizarin Red S staining, quantitative real-time polymerase chain reaction, Western blotting, immunofluorescence, and DKK-1 inhibition assays. Results PCG application significantly reduced inflammatory infiltration and stimulated reparative dentin formation in the rat pulpitis model. At the cellular level, PCG enhanced the odontogenic differentiation of DPSCs and upregulated key odontogenic markers (ALP, Runx2, DMP-1, and DSPP) at both the gene and protein levels. Mechanistically, PCG promoted the nuclear translocation of β-catenin, consistent with activation of the canonical Wnt/β-catenin signalling pathway. The pro-odontogenic effects of PCG were largely attenuated by DKK-1–mediated inhibition of canonical Wnt signalling. Conclusion PCG promoted the odontogenic differentiation of DPSCs at least in part through activation of the Wnt/β-catenin signalling pathway. These findings identify PCG as a promising modulator of odontogenic differentiation and provide mechanistic evidence supporting its further investigation for dentin-pulp repair. Clinical relevance These findings provide a biological rationale for further investigation of PCG-containing strategies for vital pulp therapy.
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高影响因子
BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR AND CELL BIOLOGY OF LIPIDS
·
2026
·Vol. 1871
·期 5
·159746
·
IF 3.8
Lang Lang,Jiaqi He,Xinwen Zhang,Kai Xu,Rui Ma,Wenge Li,Xu Yan
Background Punicalagin (PUN), the main bioactive in pomegranate peel polyphenols, plays a key therapeutic effect against diverse ailments, especially inflammatory diseases. Advanced Glycation End Products (AGEs) can disrupt lipid metabolism, trigger inflammation, and are closely linked to metabolic inflammatory diseases. Based on PUN's known protective effects, this study uses lipidomic analysis to examine its influence on AGEs-induced metabolic inflammation, providing a basis for anti-inflammatory drug research. Purpose To develop the medicinal value of PUN by studying its effects on AGEs-induced inflammation and lipid metabolism disorders. Methods RAW264.7 macrophages were first stimulated with AGEs (200 μg/mL), followed by treatment with PUN (25–100 μg/mL). Next, TNF-α and IL-1β levels were measured by ELISA. Western blotting was then performed to assess the expression of PPARγ and key proteins in the NF-κB and JNK signaling pathways, nuclear translocation of NF-κB p65 was visualized via immunofluorescence. By using the antagonist GW9662, the upstream and downstream relationship between PPARγ and NF-κB, as well as JNK, was demonstrated. Finally, non-targeted lipidomics using UPLC-Q/TOF-MS, combined with PCA and OPLS-DA multivariate analysis, identified differential lipid metabolites. Results PUN significantly suppressed AGEs-induced secretion of TNF-α and IL-1β in a concentration-dependent manner. Mechanistically, PUN upregulated PPARγ expression, inhibited the phosphorylation of IKKα/β, IκB-α, and NF-κB, reduced p-JNK, c-Jun, and c-Fos levels, and blocked nuclear translocation of p65. The use of the PPARγ antagonist GW9662 led to a re-upregulation of the phosphorylation levels of the NF-κB and JNK pathways downstream of PPARγ. The original inhibitory effect of PUN was blocked. This confirmed that the anti-inflammatory mechanism of PUN depends on the activation of PPARγ. Lipidomics analysis revealed that PUN reversed 31 dysregulated lipid metabolites induced by AGEs, with glycerophospholipid metabolism identified as the most significantly enriched pathway. Conclusion This study demonstrates that PUN alleviates AGEs-induced inflammation by restoring glycerophospholipid metabolism homeostasis, upregulating PPARγ expression, and subsequently suppressing NF-κB and JNK signaling pathways.
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DOI
PubMed
高影响因子
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