Microorganisms
·
2024
·Vol. 12
·期 9
·1871
·
IF 4.1
Lankun Yi,Mingze Cao,Xu Chen,Yubin Bai,Weiwei Wang,Xiaojuan Wei,Yuxiang Shi,Yongying Zhang,Tenghe Ma,Zhen Zhu,Jiyu Zhang
Bacterial drug resistance is becoming an increasingly serious problem, and the development of antibacterial synergists is urgently needed. Combining existing antibiotics with promising nonantibiotic agents is one strategy that has been shown to be effective at overcoming the widespread emergence of antibiotic-resistant pathogens. In this study, we investigated the antibacterial activities and mechanism of naringenin (NG) combined with amikacin (AMK) against multidrug-resistantEscherichia coli(E. coli). We first measured the fractional inhibitory concentration (FIC) of NG combined with antibiotics via the checkerboard method. The results indicated that the combination of NG and AMK had a synergistic effect onE. coliATCC 25922 andE. coliC7F3. In addition, this synergistic effect was verified by time-kill assays. Moreover, scanning electron microscopy (SEM) was used to observe cell morphology. The results showed that the cell wall ofE. coliwas destroyed. Furthermore, we assessed the leakage of alkaline phosphatase (AKP), K+, and protein. The extracellular AKP activity increased after the combinational group of 1/2MIC NG and 1/2MIC AMK, suggesting an impairment in cell wall permeability. An increase in the leakage of intracellular K+and protein indicated an increase in cell inner membrane permeability. These results revealed that NG and AMK inhibitedE. coliby damaging cell walls and membranes. In addition, PI uptake rapidly increased after treatment with NG and AMK. Confocal laser scanning microscopy (CLSM) revealed that NG caused cell wall and cell membrane damage inE. coli. In summary, our results provide a new strategy for responding to the development ofE. colidrug resistance.
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BRITISH JOURNAL OF PHARMACOLOGY
·
2024
·
IF 6.8
Chen Pan,Yuhao Xu,Zongsheng Jiang,Chengjiang Fan,Zhexi Chi,Yu Zhang,Mengmeng Miao,Yuxuan Ren,Ziyi Wu,Linbin Xu,Changqing Mei,Qingge Chen,Yang Xi,Xiaowei Chen
Background and Purpose Chemotherapy-induced peripheral neuropathy (CIPN) commonly causes neuropathic pain, but its pathogenesis remains unclear, and effective therapies are lacking. Naringenin, a natural dihydroflavonoid compound, has anti-inflammatory, anti-nociceptive and anti-tumour activities. However, the effects of naringenin on chemotherapy-induced pain and chemotherapy effectiveness remain unexplored. Experimental Approach Female and male mouse models of chemotherapy-induced pain were established using paclitaxel. Effects of naringenin were assessed on pain induced by paclitaxel or calcitonin gene-related peptide (CGRP) and on CGRP expression in dorsal root ganglia (DRG) and spinal cord tissue. Additionally, we examined peripheral macrophage infiltration, glial activation, c-fos expression, DRG neuron excitability, microglial M1/M2 polarization, and phosphorylation of spinal NF- κ B. Furthermore, we investigated the synergic effect and related mechanisms of naringenin and paclitaxel on cell survival of cancer cells in vitro. Key Results Systemic administration of naringenin attenuated paclitaxel-induced pain in both sexes. Naringenin reduced paclitaxel-enhanced CGRP expression in DRGs and the spinal cord, and alleviated CGRP-induced pain in naïve mice of both sexes. Naringenin mitigated macrophage infiltration and reversed paclitaxel-elevated c-fos expression and DRG neuron excitability. Naringenin decreased spinal glial activation and NF- κ B phosphorylation in both sexes but influenced microglial M1/M2 polarization only in females. Co-administration of naringenin with paclitaxel enhanced paclitaxel's anti-tumour effect, impeded by an apoptosis inhibitor. Conclusion and Implications Naringenin's anti-nociceptive mechanism involves CGRP signalling and neuroimmunoregulation. Furthermore, naringenin facilitates paclitaxel's anti-tumour action, possibly involving apoptosis. This study demonstrates naringenin's potential as a supplementary treatment in cancer therapy by mitigating side effects and potentiating efficacy of chemotherapy. Graphical ∎
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Food & Function
·
2019
·Vol. 10
·期 5
·2752-2765
·
IF 3.241
Li-Ming Yu,Xue Dong,Xiao-Dong Xue,Jian Zhang,Zhi Li,Hong-Jiang Wu,Zhong-Lu Yang,Yang Yang,Hui-Shan Wang
Mitochondrial dysfunction contributed greatly to myocardial ischemia-reperfusion (MI/R)-induced cardiomyocyte apoptosis. Naringenin is a flavonoid exhibiting potential protective effects on myocardial mitochondria under stress conditions. However, the detailed down-stream signaling pathway involved remains uncovered. This study was designed to elucidate naringenin's mitochondrial protective actions during MI/R with a focus on AMPK-SIRT3 signaling. Sprague-Dawley rats were administered with naringenin (50 mg kg−1 d−1) and subjected to MI/R surgery in the presence or absence of compound C (0.25 mg kg−1, Com.C, an AMPK inhibitor) co-treatment. An in vitro study was performed on H9c2 cardiomyoblasts subjected to simulated ischemia-reperfusion treatment. Before the treatment, the cells were administered with naringenin (80 μmol L−1) with or without SIRT3 siRNA/AMPK1α siRNA transfection. Naringenin improved post-reperfusion left ventricular systolic pressure and the instantaneous first derivative of left ventricular pressure, and reduced the infarction size and myocardial apoptosis index by suppressing mitochondrial oxidative stress damage (as evidenced by decreased mitochondrial cytochrome c release and oxidative markers) and enhancing mitochondrial biogenesis [as evidenced by increased NRF1, TFAM and oxidative phosphorylation subunit complexes (II, III and IV)]. These protective actions were abolished by Com.C (in vivo) or SIRT3 siRNA (in vitro) administration. Further investigation revealed that Com.C (in vivo) or AMPK1α siRNA (in vitro) markedly suppressed PGC-1α and SIRT3 levels while SIRT3 siRNA (in vitro) inhibited SIRT3 expression without significantly changing AMPK phosphorylation and PGC-1α levels. Taken together, we found that naringenin directly inhibits mitochondrial oxidative stress damage and preserves mitochondrial biogenesis, thus attenuating MI/R injury. Importantly, AMPK-SIRT3 signaling played a key role in this process.
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GENERAL PHYSIOLOGY AND BIOPHYSICS
·
2024
·Vol. 43
·期 1
·13-23
·
IF 1.3
Xiao Jin,Ling Jin,Bingxin Wu,Danping Xu
Myocardial ischemia/reperfusion (I/R) causes serious threats to human life. Naringenin, a polyphenolic compound naturally occurring in citrus fruit, has cardioprotective effects against myocardial I/R injury. Besides, miR-24-3p is also reported to have cardioprotective effects. We intended to explore whether the cardioprotective effects of naringenin relate to miR-24-3p and its underlying mechanism. In this study, we used an in vivo rat myocardial I/R model and an in vitro cardiomyocyte H9c2 hypoxia/reoxygenation (H/R) model. Myocardial injury was detected by hematoxylin-eosin staining and ELISA for creatine kinase (CK), malondialdehyde (MDA), and lactate dehydrogenase (LDH). miR-24-3p and cell death inducing p53 target 1 (Cdip1) mRNA expressions were examined by RT-PCR. We find that naringenin pretreatment significantly relieves myocardial I/R injury, reduces LDH, CD, and MDA levels, and increases miR-24-3p expression. Furthermore, miR-24-3p alleviates myocardial I/R injury partially through regulating Cdip1. Moreover, naringenin protects myocardial I/R injury partially by regulating miR-24-3p to inhibit Cdip1 expression. In conclusion, our data suggest naringenin protects myocardial I/R injury partially through miR-24-3p/Cdip1 axis.
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JOURNAL OF MICROBIOLOGY AND BIOTECHNOLOGY
·
2025
·
IF 3.1
Jiahui Sun,Luyao Shi,Fan Xu,Hanyan Sun,Yitong Liu,Jiangyun Sun,Qingxin Zhou
Colorectal cancer (CRC) is a worldwide health issue. It causes illness and death in millions of people each year. A positive correlation has been observed between the intake of dietary fat and the development of CRC. The composition of gut microbiota exhibits a significant correlation with pathophysiologic processes in intestine. Clinical treatment remains inadequate due to the complex pathogenic mechanisms of CRC triggered by a high-fat diet (HFD). Naringenin, a flavonoid from grapefruit, has anti-cancer activity. Our findings suggest that naringenin enhances gut microbiota diversity by increasing the abundance of beneficial bacterial species while reducing opportunistic pathogenic bacteria. The fecal microbiota transplantation assay (FMT) demonstrated that the anti-HFD-CRC activity of naringenin depended on the gut microbiota. Furthermore, naringenin antagonized the IL-6/STAT3 pathway. These results suggest that naringenin may be a potential treatment for HFD-CRC.
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ACS Applied Bio Materials
·
2026
·
IF 4.7
Yingying Du,Lin Wang,Yi Ouyang,Qun Chen,Ziwei Liu,Zhimei Liu
Quercetin (Que) and naringenin (Nar) are natural compounds with potent antioxidant and anti-inflammatory activities, showing promise for alleviating ultraviolet B (UVB)-induced skin photoaging. The presence or absence of a C═C bond in the C-ring defines whether the compound is a flavonol or a flavanone. To overcome poor water solubility and low bioavailability of the two flavonoids, we prepared inclusion complexes using β-cyclodextrin (β-CD), hydroxyethyl-β-cyclodextrin (HE-β-CD), and hydroxypropyl-β-CD (HP-β-CD). These complexes leverage the cyclodextrins’ hydrophilic exterior and hydrophobic interior to encapsulate Que and Nar, respectively. Through integrated analyses─including molecular docking, phase solubility studies, characterization (UV, Fourier-transform infrared (FT-IR), X-ray diffraction (XRD), scanning electron microscopy (SEM), and NMR), solubility tests, and antioxidant (2,2-diphenyl-1-picrylhydrazyl (DPPH)) assays─we systematically elucidated the structure–activity relationships of these flavonoid–cyclodextrin interactions. The therapeutic potential was further evaluated in a UVB-induced mouse model of skin photoaging. Results confirmed the spontaneous formation of stable 1:1 molar ratio inclusion complexes between the flavonoids and cyclodextrins. The enhancement of complex stability, water solubility, and antioxidant activity consistently followed the order: HP-β-CD > HE-β-CD > β-CD. Owing to Que’s conjugated planar structure, it exhibited weaker binding to β-CD than did Nar. However, Que formed more stable complexes with HE-β-CD and HP-β-CD than Nar did. In vivo, the Que/HP-β-CD complex demonstrated superior efficacy, most effectively reducing malondialdehyde (MDA) levels, alleviating epidermal hyperplasia, and increasing collagen fiber content. Furthermore, the inclusion complexes amplified the regulatory effects of Que and Nar on mitogen-activated protein kinase (MAPK) and TGF-β/Smad pathways: they enhanced the downregulation of p-p38 and MMP-1 to inhibit collagen degradation and promoted the upregulation of Smad2/3 and COL1A1 to stimulate collagen synthesis. In conclusion, the β-cyclodextrin inclusion complexes of flavonoids, designed based on structure–activity relationship studies, significantly improve the compounds’ solubility, stability, and bioactivity. This leads to enhanced protective efficacy against UVB-induced photodamage through the concurrent modulation of multiple signaling pathways.
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Aquaculture Reports
·
2026
·
IF 3.7
Dexiang Feng,Xiaotong Si,Wenxuan Liu,Pengwei Xun,Qianqian Huang,Mingzhu Liu,Ming Li
Naringenin (NGN), a flavonoid compound abundantly found in citrus fruits, exhibits anti-inflammatory, anti-oxidative activities, and hypolipidemic properties. However, nowadays, NGN is mainly used to inhibit the occurrence of viral diseases in aquatic animals by injection as an immunosuppressant, and its safety and other physiological effects as a feed additive have not been sufficiently investigated. This study elucidates how naringenin (NGN) mitigates the negative impacts exerted by a high-fat diet (HFD) on Largemouth bass ( Micropterus salmoides ) from hepatic and intestinal perspectives. After an 8-week feeding trial, the NGN groups had a significant effect on growth performance compared to the HFD group, and significantly decreased the lipid content of the whole body. Secondly, NGN significantly decreased the levels of triglycerides and total cholesterol in serum compared with the HFD group, down-regulated the lipogenesis-related genes, and significantly up-regulated the lipolysis-related genes. Furthermore, hepatic injury markers alanine transaminase and aspartate transaminase were also significantly decreased. Additionally, NGN significantly enhanced the antioxidant capacity of the liver, down-regulated the gene expression of pro-inflammatory factors, and up-regulated the anti-inflammatory factors. There were remarkable changes in the structure of the gut microbiota, where the biomarker of the Na1 group was Dyella , and the main ones in the Na2 group were Asinibacterium , Methylovirgula , Mesorhizobium, and Meiothermus . The function of the gut microbiota in the NGN was more enriched in the fatty acid biosynthesis pathway compared to the high-fat diet. To conclude, the supplementation of NGN to HFD can significantly reduce hepatic lipid deposition and alleviate liver damage, as well as improve gut health status. Among them, the addition of 0.007 % naringenin exhibited a better effect. The results of this study will be used to help reduce the negative effects of an HFD within the aquaculture sector and hold the potential to be regarded as a promising eco-friendly feed additive for aquaculture.
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FOOD AND CHEMICAL TOXICOLOGY
·
2023
·
IF 4.3
Shuai Liu,Xintao Gao,Yulan Yin,Jing Wang,Kehong Dong,Dayong Shi,Xiaochen Wu,Chuanlong Guo
Silk fibroin (SF) has excellent biocompatibility and biodegradability as a biomaterial. The purity and molecular weight distribution of silk fibroin peptide (SFP) make it more suitable for medical application. In this study, SFP nanofibers (molecular weight ∼30kD) were prepared through CaCl 2 /H 2 O/C 2 H 5 OH solution decomposition and dialysis, and adsorbed naringenin (NGN) to obtain SFP/NGN NFs. In vitro results showed that SFP/NGN NFs increased the antioxidant activity of NGN and protected HK-2 cells from cisplatin-induced damage. In vivo results also showed that SFP/NGN NFs protected mice from cisplatin-induced acute kidney injury (AKI). The mechanism results showed that cisplatin induced mitochondrial damage, as well as increased mitophagy and mtDNA release, which activated the cGAS-STING pathway and induced the expression of inflammatory factors such as IL-6 and TNF-α. Interestingly, SFP/NGN NFs further activated mitophagy and inhibited mtDNA release and cGAS-STING pathway. Demonstrated that mitophagy-mtDNA-cGAS-STING signal axis was involved in the kidney protection mechanism of SFP/NGN NFs. In conclusion, our study confirmed that SFP/NGN NFs are candidates for protection of cisplatin-induced AKI, which is worthy of further study.
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JOURNAL OF MOLECULAR LIQUIDS
·
2020
·
IF 5.065
Xingang Lv,Qilei Wang,Lang-Hong Wang,Er-Fang Ren,Deming Gong
In this work, the inhibitory effect of two citrus flavonoids naringenin and hesperetin on human purine nucleoside phosphorylase (hPNP) and their binding mechanism were evaluated. Results from enzymatic kinetics revealed that naringenin and hesperetin reversibly inhibited hPNP via a mixed-type manner with IC 50 values of 4.83 × 10 −4 M and 5.32 × 10 −4 M, respectively. Analysis of molecular modeling revealed that both naringenin and hesperetin bound directly into the active site by generating multiple forces including hydrogen bonding , π–π and π-Alkyl interactions with His64, Glu201, Ser220, His257, Phe200 and Val217 residues of hPNP, which caused the inhibition of hPNP activity. Moreover, conformational analysis by three-dimension fluorescence, circular dichroism and atomic force microscopy revealed that the binding of naringenin and hesperetin to hPNP induced changes in the microenvironment, secondary structure and morphology of hPNP. These results suggested that occupying the active site and enzymatic conformational perturbation induced by naringenin and hesperetin are the main reasons for reducing the inhibition of hPNP activity, which would be helpful in understanding the inhibitory mechanism of naringenin and hesperetin against hPNP.
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Food Chemistry-X
·
2024
·
IF 6.5
Xiumei Chen,Yingying Sheng,Jinxin Che,Okwong Oketch Reymick,Nengguo Tao
Grapefruit ( Citrus × paradisi Macf.) peel, a by-product of the citrus-processing industry, possesses an important economic value due to the richness of bioactive compounds. In this study, boron-linked covalent organic frameworks integrated with molecularly imprinted polymers (CMIPs) were developed via a facile one-pot bulk polymerization approach for the selective extraction of naringenin from grapefruit peel extract. The obtained CMIPs possessed a three-dimensional network structure with uniform pore size distribution, large surface areas (476 m 2 /g), and high crystallinity. Benefiting from the hybrid functional monomer APTES-MAA, the acylamino group can coordinate with the boronate ligands of the boroxine-based framework to form B-N bands, facilitating the integration of imprinted cavities with the aromatic skeleton. The composite materials exhibited a high adsorption capacity of 153.65 mg/g, and a short adsorption equilibrium time of 30 min for naringenin, together with favorable selectivity towards other flavonoid analogues. Additionally, the CMIPs captured the template molecules through π–π* interaction and hydrogen bonding, as verified by FT-IR and XPS. Furthermore, they had good performance when employed to enrich naringenin in grapefruit peels extract compared with the common adsorbent materials including AB-8, D101, cationic exchange resin, and active carbon. This research highlights the potential of CMIPs composite materials as a promising alternative adsorbent for naringenin extraction from grapefruit peel.
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FOOD HYDROCOLLOIDS
·
2024
·
IF 11
Ying-Ying Chen,Qiang-Ming Li,Li-Hua Pan,Jian-Ping Luo,Xue-Ying Li,Xue-Qiang Zha
Naringenin (Nar) is a natural flavonoid with diverse health-promoting benefits. However, the bioavailability of Nar is significantly restricted due to its poor water-solubility, instability under physiological conditions, and limited absorption profile. In this study, a shellac-quinoa protein isolate (QPI) binary nanocomplex (SQP) was fabricated using the pH-shifting method for effectively delivering Nar. Isothermal titration calorimetry (ITC) and analysis of inner interactive forces revealed that the complexation between QPI and shellac was primarily driven by electrostatic and hydrophobic forces. Subsequently, Nar was successfully encapsulated within the stable and uniform SQP nanocomplex (Nar@SQP), achieving a high encapsulation capacity (94.52 % encapsulation efficiency and 14.68 % loading capacity). Meanwhile, the Nar@SQP nanoparticle exhibited excellent stability against pH, ionic strength, and long-term storage. Moreover, it also demonstrated sustained and slow-release characteristics during simulated gastrointestinal digestion. Compared to free Nar, the safe Nar@SQP nanoparticle effectively facilitated the cellular uptake of encapsulated Nar by Caco-2 cells, suggesting that Nar@SQP has a good potential to improve the bioavailability of Nar. Hence, these findings indicated that the developed Nar@SQP nanoparticle might hold significant promise as a nano-delivery system for hydrophobic bioactive nutrients, like Nar.
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Frontiers in Pharmacology
·
2024
·
IF 4.4
Shi Yaning,Gao Zhixin,Xu Bing,Mao Junbing,Wang Yue,Liu Zongping,Wang Jicang
Cadmium (Cd) is a highly hazardous toxic substance that can cause serious harm to animals. Previous studies have indicated that cadmium chloride (CdCl2) can damage organs, such as the liver, ovaries, and testicles. Naringenin (Nar) represents a flavonoid with various properties that promote the alleviation of Cd-induced damage. In this experiment, 60 chickens were divided into the control group, 150 mg/kg CdCl2 treatment group, 250 mg/kg Nar treatment group, and 150 mg/kg CdCl2 + 250 mg/kg Nar co-treatment group, which were treated for 8 weeks. Kidney tissues samples were collected to investigate kidney function, including oxidative stress (OS), endoplasmic reticulum (ER) stress, and autophagy activity. Experimental results showed the decreased weight of chickens and increased relative weight of their kidneys after CdCl2 treatment. The increase in NAG, BUN, Cr, and UA activities, as well as the increase in MDA and GSH contents, and the decrease activities of T-AOC, SOD, and CAT in the kidney, manifested renal injury by OS in the chickens. TUNEL staining revealed that CdCl2 induced apoptosis in renal cells. CdCl2 upregulates the mRNA and protein expression levels of GRP78, PERK, eIF2α, ATF4, ATF6, CHOP, and LC3, and inhibited the mRNA and protein expression levels of P62 proteins, which leads to ER stress and autophagy. The CdCl2 + Nar co-treatment group exhibited alleviated CdCl2-induced kidney injury, OS, ER stress, and autophagy. Research has demonstrated that Nar reduces CdCl2-induced kidney injury through alleviation of OS, ER stress, and autophagy.
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