Foods
·
2024
·Vol. 13
·期 23
·3797
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IF 4.7
Chenmeng Song,Wei Zheng,Chengyi Song,Houfeng Zhou,Jengyuan Yao
Background: Kaempferol (KPF), a flavonoid abundant in edible plants, possesses potent anti-inflammatory and antioxidant properties beneficial with notable health benefits. Objective: To evaluate the protective effects of KPF on metabolic disturbances and pancreatic damage in a Type 1 diabetes mellitus (T1DM) mouse model. Methods: Male C57BL/6 mice were divided into normal, T1DM, T1DM + KPF 25 mg/kg, and T1DM + KPF 50 mg/kg groups. T1DM was induced by streptozotocin (STZ). KPF was administered via intraperitoneal injection for 2 weeks. After 4 weeks from the start, metabolic parameters, pancreatic histology, and plasma metabolites were analyzed. Network pharmacology and molecular docking identified key targets and pathways. In vitro, INS-1 cells were used to assess reactive oxygen species (ROS) production and apoptosis. Results: KPF significantly reduced blood glucose (GLU) and triglyceride (TG) levels, increased high-density lipoprotein (HDL) levels, and preserved pancreatic β-cell structure. Metabolomics revealed changes in energy metabolism and oxidative stress-related metabolites. Network analysis highlighted the PI3K/AKT/mTOR pathway, with strong binding affinities to targets such as AKT1. In vitro, KPF decreased ROS production in INS-1 cells; this effect was reversed by a PI3K/AKT inhibitor. KPF also reduced apoptosis in INS-1 cells. Conclusions: KPF ameliorates metabolic disturbances and pancreatic damage in T1DM mice, suggesting potential as a functional food ingredient for diabetes management.
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Frontiers in Cell and Developmental Biology
·
2024
·
IF 4.6
Zhao Liusha,Luo Ting,Zhang Hong,Fan Xinxin,Zhang Qiaoqiao,Chen Haiyang
Introduction: Intestinal stem cells (ISCs) are crucial for tissue repair and homeostasis because of their ability to self-renew and differentiate. However, their functionality declines significantly with age, resulting in reduced tissue regeneration and a higher risk of age-related diseases. Addressing this decline in ISC performance during aging presents a substantial challenge. The specific impact of nutrients or dietary elements on ISC adaptive resizing is urgent to explore.Methods: Drosophila ISCs are an ideal model for studying development and aging because of their genetic richness, ease of manipulation, and similarity to mammalian tissues. As the primary mitotically active cells in the Drosophila gut, ISCs are flexible in response to dietary and stress signals. Manipulating signaling pathways or dietary restrictions has shown promise in regulating ISC functions and extending lifespan in flies, these approaches face broader applications for aging research.Results: Kaempferol is well-regarded for its antioxidant, anti-inflammatory, and potential anticancer effects. However, its impacts on ISCs and the associated mechanisms remain inadequately understood. Our findings indicate that Kaempferol accelerates gut recovery after damage and improves the organism’s stress tolerance. Moreover, Kaempferol suppresses the hyperproliferation of aging ISCs in Drosophila. Further investigation revealed that the regulatory effects of Kaempferol on ISCs are mediated through the reduction of endoplasmic reticulum (ER) stress in aging flies and the modulation of excessive reactive oxygen species (ROS) levels via ER-stress pathways. Furthermore, Kaempferol exerts regulatory effects on the insulin signaling pathway, thereby contributing to the attenuation of ISC senescence.Discussion: This study reveals that Kaempferol promotes intestinal homeostasis and longevity in aging flies by targeting ER stress and insulin signaling pathways, though the exact molecular mechanisms require further exploration. Future research will aim to dissect the downstream signaling events involved in these pathways to better understand how Kaempferol exerts its protective effects at the molecular level.
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COLLOIDS AND SURFACES A-PHYSICOCHEMICAL AND ENGINEERING ASPECTS
·
2026
·
IF 5.4
Xiuqing Guan,Ziwei Ye,Xin Lei,Xinyan Wen,Jie Duan,Xianrui Chen,Lin Wang,Jie Pang
Flower-like KGZn superstructures formed by sequential coordination assembly. • KGZn enhances barrier, mechanical, and UV-blocking properties of KC films. • KC-KGZn films show DPPH (43.40%) and ABTS (97.67%) scavenging activities. • KC-KGZn films exhibit > 92% antibacterial ratios against E. coli , S. aureus , and S. cerevisiae . • KC-KGZn films extend blueberry shelf life to 15 days at 25 °C. The challenge of spoilage and waste in fruits is creating a strong demand for the development of green and efficient active packaging materials. This work presents a flower-like kaempferol–gallic acid–Zn coordination superstructure (KGZn) synthesized via coordination-driven assembly. KGZn was incorporated into a film matrix composed of konjac glucomannan and carboxymethyl chitosan (KGM/CMCS, denoted as KC), yielding the KC-KGZn composite film. Serving as a multifunctional agent, KGZn significantly improves the physicochemical properties of the composite film, enhancing its barrier performance and mechanical properties. Furthermore, the composite film exhibits excellent antioxidant activity, with DPPH and ABTS scavenging rates reaching 43.40 ± 2.10% and 97.67 ± 0.67%, respectively, as well as potent antimicrobial activity, showing inhibition ratios of 92.15%, 100%, and 98.66% against Escherichia coli , Staphylococcus aureus , and Saccharomyces cerevisiae , respectively. In blueberry preservation tests, the KC-KGZn composite film effectively slowed down fruit weight loss and firmness degradation, maintained soluble solids content, and preserved desirable sensory quality after 15 days of storage at 25 °C. These results indicate that the introduction of this flower-like superstructure material is an effective strategy for fabricating high-performance food packaging films, while also promoting the development of metal-polyphenol functional fillers. Download: Download high-res image (173KB) Download: Download full-size image
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FOOD AND CHEMICAL TOXICOLOGY
·
2023
·
IF 4.3
Xueqin Wang,Zhenzhen Cui,Yuan Luo,Yu Huang,Xinbin Yang
Xanthine oxidase (XO), a key enzyme in purine catabolism, catalyzes the oxidation of xanthine to uric acid in the body, but overproduction of uric acid may lead to hyperuricemia . This study aims to investigate in vitro XO inhibitory and in vivo anti-hyperuricemic properties of sodium kaempferol-3′-sulfonate (KS). The kinetic analysis indicates that KS is a reversible competitive inhibitor and has significant inhibitory effects on XO activity with an IC 50 value of 0.338 μM. Fluorescence spectra suggested that KS could cause fluorescence quenching and conformational changes of XO due to the formation of a KS-XO complex. Molecular docking studies demonstrated that KS interacted with several amino acid residues of XO by the π-π stacking, hydrogen bonds , and hydrophobic interactions. The inhibitory mechanism of KS on XO activity might be the insertion of KS into the active site of XO to prevent the entrance of the substrate xanthine and induce conformational changes of XO. The results carried out in hyperuricemic mice showed that KS reduced serum XO activity, serum uric acid (UA), creatinine (CRE), and urea nitrogen (BUN) levels, as well as alleviating renal histopathological injury. These findings suggest that KS may be a new potent XO inhibitor against hyperuricemia-related diseases.
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iScience
·
2024
·Vol. 27
·期 11
·111186
·
IF 4.6
Yan Huang,Cantao Li,Wenjing Xu,Fenfen Li,Ying Hua,Changyu Xu,Chenxi Wu,Yihuan Wang,Xiaoxi Zhang,Daozong Xia
Hyperuricemia (HUA), caused by purine disorders, can lead to gouty arthritis (GA). Kaempferol (KPF), a natural flavonoid, has anti-inflammatory properties, though its mechanism in treating HUA combined with GA remains unclear. This study used a mouse model of HUA combined with GA and in vitro models with HK-2 and THP-1 cells to explore KPF’s effects. Cells were treated with KPF or inhibitors of ABCG2, ROS, NLRP3 inflammasome, and nuclear factor κB (NF-κB) pathway. Quantitative assays measured uric acid (UA), creatinine, oxidative stress biomarkers, and pro-inflammatory cytokines. Histopathological analyses showed KPF improved renal and joint inflammation caused by HUA and GA. KPF alleviated oxidative stress, reduced pro-inflammatory cytokines, and regulated UA levels through the modulation of urate transporters, NLRP3 inflammasome, and NF-κB pathway. KPF’s actions, partly mediated by ROS reduction, suggest it is a promising candidate for treating HUA combined with GA.
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INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
·
2025
·Vol. 26
·期 14
·6666
·
IF 4.9
Siqi Zhang,Fei Tang,Zhe Zhou,Linhui Li,Yang Tang,Kaiwen Fu,Yang Tan,Ling Li
Liver fibrosis remains a critical health concern with limited therapeutic options. Kaempferol (Kae) is a natural flavonoid widely present in natural plants, yet its role in modulating gut–liver axis interactions during fibrosis is unexplored. This study investigates the hepatoprotective effects of Kae on alleviating carbon tetrachloride (CCl4)-induced liver fibrosis, and its underlying mechanisms, focusing on oxidative stress, gut microbiota, and short-chain fatty acids (SCFAs), are revealed. A mouse model of hepatic fibrosis was built by the subcutaneous injection of CCl4. Meanwhile, Kae was administered by gavage at doses of 25, 50, and 100 mg/kg body weight. Serum biomarkers, liver histopathology, oxidative damage markers, and nuclear factor erythroid 2-related factor 2 (Nrf2)/kelch-like ECH-associated protein 1 (Keap1)/heme oxygenase 1 (HO-1) signaling were analyzed. AML12 hepatocytes were pretreated with Kae or SCFAs (acetate, propionate, butyrate) before H2O2-induced oxidative injury. The changes in gut microbiota and the levels of SCFAs were assessed via 16S rRNA sequencing and GC-MS, respectively. Kae effectively alleviated the destruction of the liver morphology and tissue structure, reduced the infiltration of inflammatory cells, collagen deposition in the liver, and the expression of fibrotic factors, and downregulated the oxidative stress level in the liver of mice with liver fibrosis by activating the Nrf2/Keap1/HO-1 pathway (p< 0.05 or 0.01). In vitro, Kae significantly mitigated H2O2-induced cytotoxicity and oxidative damage (p< 0.05 or 0.01). Furthermore, Kae restored gut microbiota diversity, increased beneficial genera (e.g.,Lactobacillus), and elevated both intestinal and hepatic SCFA levels (p< 0.01). The discrepant SCFA pretreatment similarly protected AML12 cells by activating Nrf2 signaling (p< 0.05 or 0.01). Our research suggests that Kae could inhibit CCl4-induced liver fibrosis by restoring the levels of intestinal metabolite SCFAs to reduce oxidative damage.
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Natural Product Communications
·
2024
·
IF 1.5
Zhang-lin Pu,Chi Zhang,Qian Yan,Zhou Liang,Zhi-Wei Xu,Ji-hu Wei,Hua Liu,Feng Chen
Objective: We explore the pharmacodynamic targets of kaempferol in treating osteoporosis using transcriptomics and animal experiment. Methods: Firstly, we constructed an ovariectomized rat model (OVX). The anti-osteoporosis effect of kaempferol was evaluated by bone mineral density (BMD) and hematoxylin-eosin staining comprehensively. Moreover, differential genes between groups were screened by RNA sequencing technology (RNA-seq) for transcriptomics and Gene Ontology and Kyoto Encyclopedia of Genes and Genomes pathways enrichment analysis were performed. Finally, partial results of transcriptomics were verified to detect the expression of the relevant gene expression by immunohistochemistry. Results: The pharmacodynamic findings indicated that the administration of kaempferol resulted in an elevation in BMD (P < .01) and a notable enhancement in tibia microstructural indices in the experimental rats (P < .01). The transcriptomic analysis revealed that NTN1, LTBP4, GSN, and EBF1 were identified as the principal targets for therapeutic intervention in osteoporosis. The results of animal experiments showed that kaempferol promoted osteogenesis and inhibited bone resorption by downregulating the protein expression of NTN1, LTBP4, GSN, and EBF1 (P < .01). Conclusion: Kaempferol enhances BMD levels, retards tibial bone loss with structural deterioration in OVX model rats, and promotes bone formation while curbing bone resorption through NTN1, LTBP4, GSN, and EBF1 protein down-regulation.
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INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
·
2019
·Vol. 20
·期 4
·975
·
IF 4.183
Sui-Ping Deng,Yi-Li Yang,Xing-Xing Cheng,Wen-Rong Li,Ji-Ye Cai
Kaempferol (Kae) is a natural flavonoid with potent antioxidant activity, but its therapeutic use is limited by its low aqueous solubility. Here, a series of Kae derivatives were synthesized to improve Kae dissolution property in water and antioxidant activity. These compounds included sulfonated Kae (Kae-SO3), gallium (Ga) complexes with Kae (Kae-Ga) and Kae-SO3(Kae-SO3-Ga). The compound structures were characterized by high-resolution mass spectrometry (HRMS), nuclear magnetic resonance (NMR) spectroscopy, ultraviolet-visible (UV-Vis) spectroscopy, Fourier transform infrared (FT-IR) spectroscopy and thermal methods (TG/DSC). The results showed that a sulfonic group (-SO3) was successfully tethered on the C3’ of Kae to form Kae-SO3. And in the metal complexation, 4-CO and 3-OH of the ligand participated in the coordination with Ga(III). The metal-to-ligand ratio 1:2 was suggested for both complexes. Interestingly, Kae-SO3-Ga was obviously superior to other compounds in terms of overcoming the poor water-solubility of free Kae, and the solubility of Kae-SO3-Ga was about 300-fold higher than that of Kae-Ga. Furthermore, the evaluation of antioxidant activities in vitro was carried out for Kae derivatives by using α,α-diphenyl-β-picrylhydrazyl (DPPH) and 2,2’-azino-bis(3-ethylbenzo-thiazoline-6-sulfonic acid) diammonium salt (ABTS) free radical scavenging. The results showed that Kae-SO3-Ga was also optimal for scavenging free radicals in a dose-dependent manner. These data demonstrate that sulfonate kaempferol-gallium complex has a promising future as a potential antioxidant and as a potential therapeutic agent for further biomedical studies.
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JOURNAL OF NANOBIOTECHNOLOGY
·
2026
·
IF 15
Quan Liao,Shichao Zhang,Yuhan Xie,Qidan Tan,Tengfei Li,Shushuai Yang,Chenglong Xu,Zhouting Tuo,Rui Yao,Longchao Zhang,Haiwen Zhou,Yuanjiong Qi,Shiyong Qi
Background Acute kidney injury (AKI) remains a major clinical challenge and is largely driven by excessive oxidative stress, inflammatory responses, and tubular cell apoptosis. However, effective therapeutic strategies that simultaneously target these pathological processes are still lacking. Results We developed a pH-responsive ultrasmall Fe–kaempferol (Fe–Kae) nanoplatform with coordinated antioxidant and anti-inflammatory activities for AKI treatment. Owing to their ultrasmall size and pH-responsive properties, Fe–Kae nanoparticles preferentially accumulated in injured renal tissues and exhibited robust renoprotective effects in multiple murine AKI models, including ischemia–reperfusion injury, cisplatin-induced nephrotoxicity, and calcium oxalate–induced kidney injury. Integrated transcriptomic and metabolomic analyses of ischemia–reperfusion–injured kidneys revealed that Fe–Kae treatment markedly enhanced efferocytosis-associated pathways and induced coordinated metabolic reprogramming, characterized by optimized tricarboxylic acid cycle activity and enhanced glutathione metabolism. Conclusions This study establishes a nanomedicine-based therapeutic strategy that couples efferocytosis enhancement with metabolic reprogramming to achieve effective renoprotection. Our findings highlight pH-responsive ultrasmall metal–polyphenol nanoplatforms as a promising paradigm for the treatment of AKI. Graphical Open in a new tab Graphical Supplementary Information The online version contains supplementary material available at 10.1186/s12951-026-04534-8.
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Materials Today Communications
·
2025
·
IF 4.5
Biying Zhong,Dingjun Wang,Xiaotong Lai,Xiao Huang,Qiaowen Wang,Xinghan Ren,Xinyue Shen,Li Liu,Tiantian Liu
In recent years, the burden of disease caused by Staphylococcus aureus and Escherichia coli infections has been significant. Currently, the development of antibiotics faces severe challenges, as the long-term misuse of traditional antibiotics has accelerated the evolution of resistance, while the pace of novel drug development lags far behind the rate of bacterial evolution. Therefore, the development of new antibacterial agents is urgently needed. This study presents a metal-organic framework composite material loaded with zinc oxide and kaempferol (MIL-101(Fe)@Zn-KF). The prepared material was characterized using Fourier-transform infrared spectroscopy (FTIR), X-ray diffraction (XRD), ultraviolet-visible spectrophotometry (UV-Vis), scanning electron microscopy (SEM), energy-dispersive X-ray spectroscopy (EDS) and zeta potential analysis. Peroxidase-like activity, biosafety and antioxidant property of the composite were evaluated. The in vitro antibacterial effect of the composite against Staphylococcus aureus and Escherichia coli was investigated using the plate coating method and bacterial growth curves experiment. The synthesized material exhibited multifunctionality, such as enzyme-like activity, antibacterial property and antioxidant capacity. Compared to MIL-101(Fe)@Zn, MIL-101(Fe) and kaempferol alone, the MIL-101(Fe)@Zn-KF composite demonstrated superior antibacterial effect, with inhibition rate of 98.76% and 98.34% against Staphylococcus aureus and Escherichia coli , respectively. MIL-101(Fe)@Zn-KF was able to catalyze hydrogen peroxide to generate reactive oxygen species, which synergized with the composite itself to exert bactericidal effect. Systematic evaluation of the cytotoxicity and hemolytic effect of MIL-101(Fe)@Zn-KF revealed the excellent biosafety and clinical potential of the composite. In summary, the composite material synthesized in this study combined peroxidase-like activity, antibacterial performance, antioxidant capacity and excellent biocompatibility, providing new insights for the development of efficient and safe antibacterial materials.
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CURRENT ISSUES IN MOLECULAR BIOLOGY
·
2025
·Vol. 47
·期 6
·450
·
IF 3
Qiming Miao,Lu Sun,Jiayuan Wu,Xinyue Zhu,Juer Liu,Roger Ruan,Guangwei Huang,Shengquan Mi,Yanling Cheng
The advancement of modern lifestyles has precipitated excessive consumption of energy-dense foods, driving the escalating global burden of lipid metabolism dysregulation-related pathologies—including obesity, type 2 diabetes mellitus (T2DM), non-alcoholic fatty liver disease (NAFLD), and cardiovascular disorders—which collectively pose a formidable challenge to global public health systems. The almond hull, as a by-product of almond processing, is rich in polyphenolic compounds with demonstrated antioxidant, anti-inflammatory, and lipid-lowering potential, though its precise hypo-lipidemic mechanisms remain elusive. In this study, polyphenols were extracted from almond hulls using 50% ethanol with ultrasound-assisted extraction, followed by preliminary purification via solvent partitioning. The ethyl acetate fraction was analyzed by liquid chromatography–mass spectrometry (LC-MS). Network pharmacology and molecular docking were employed to investigate the interactions between key bioactive constituents (e.g., quercetin, baicalein, and kaempferol) and targets in lipid metabolism-related pathways. Molecular dynamics (MD) simulations further evaluated the stability of the lowest-energy complexes. Results revealed that the ethyl acetate fraction exhibited potent pancreatic lipase inhibitory activity (IC50 = 204.2 µg/mL). At 0.1 mg/mL after 24 h treatment, it significantly reduced free fatty acids (FFAs)-induced intracellular triglyceride accumulation (p< 0.01) and enhanced cellular antioxidant capacity. Network pharmacology and in vitro studies suggest almond hull extract modulates PI3K-AKT signaling and improves insulin resistance, demonstrating lipid-lowering effects. These findings support its potential in functional foods and pharmaceuticals, though further in vivo validation and mechanistic investigations are required.
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JOURNAL OF MOLECULAR STRUCTURE
·
2023
·
IF 3.8
Huiling Zhou,Chenxin Duan,Huimin Qin,Chaonan Huang,Jingxuan Hou,Yanming Chen,Jin Zhu,Cangcang Xu,Jian Jin,Tao Zhuang
ABSTRACT Palbociclib (PAL), a highly selective inhibitor of cell cycle protein-dependent kinases (CDK) 4/6, is primarily used for treating advanced breast cancer. However, the use of PAL has been limited by its poor tabletability and dose-related toxic side effects. In this study, to improve the tabletability of PAL and reduce its effective dose, a flavonoid–kaempferol (KAE) was selected as the coformer to synthesize cocrystal with PAL. The novel cocrystal PAL-KAE was prepared by antisolvent cocrystallization and characterized by various techniques including X-ray diffraction (SCXRD and PXRD), thermal analysis (DSC and TG), Fourier transform infrared spectroscopy (FT-IR), scanning electron microscopy (SEM), Hirshfeld surface (HS), HOMO−LUMO analysis, and molecular electrostatic potential (MEP). Powder compaction experiments indicated that PAL-KAE cocrystal significantly improved the tabletability of PAL. The cytotoxicity test suggested that PAL-KAE also exerted synergistic antitumor effect against human ovarian cancer cell line OVCAR3 in MTT assay. Docking results indicated that PAL-KAE had lower binding energy with CDK 6 than PAL. Furthermore, the cocrystal PAL-KAE exhibits excellent stability in long-term testing, accelerated testing and stressing test. This paper provides a promising strategy for improving the tabletability of PAL and enhancing its anticancer activity, thus reducing the dose-related side effects of PAL.
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