Advanced Healthcare Materials
·
2026
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IF 11
Xinyue Wei,Peng Guan,Jie Fang,Jinjing Yin,Ziao Xu,Chuanrun Li,Huchuan Wang
Diabetic wound dressings require strong adhesion, painless removal and effective treatment against chronic inflammation. Herein, a multifunctional hydrogel KAE@ZIF-8/Mg 2+ /PDA-NIPAM-PAM (abbreviated as KAE@ZIF-8/Mg 2+ /PNP) was prepared by copolymerizing dopamine, N-isopropylacrylamide, and acrylamide with kaempferol-loaded ZIF-8 nanoparticles. The hydrogel integrates thermosensitive gelation and bioadhesion delivery to treat diabetic wounds. It forms gel within 1 min at 37°C with reliable tissue adhesion, while adhesion drops sharply after 20 min immersion at 10°C for trauma-free detachment. This hydrogel achieves pH-responsive drug release, with 24 h cumulative KAE release rates of 49.8 ± 1.33% at pH 5.3 and 18.1 ± 0.82% at pH 7.4. It possesses excellent hemostatic, pro-angiogenic, anti-inflammatory, and antioxidant properties. Moreover, the hydrogel exhibits a compressive modulus of 89.98 kPa and favorable cytocompatibility, maintaining over 90% viability of NIH/3T3 fibroblasts.
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Food & Function
·
2023
·Vol. 14
·期 4
·1884-1896
·
IF 6.1
Huiyi Li,Qiqing Weng,Shuai Gong,Weixian Zhang,Jiaqi Wang,Yuqiao Huang,Yuanjun Li,Jiao Guo,Tian Lan
Acetaminophen (APAP)-induced liver injury (AILI) has become a growing public health problem. Ferroptosis, an iron-dependent form of cell death associated with lipid peroxide accumulation, has been recently implicated in AILI. The activation of the Nrf2 signaling pathway is a potential therapy for AILI. Kaempferol (KA), a flavonoid widely existing in edible plants, has been reported to exert profound anti-inflammatory and antioxidant activities. This study aimed to investigate whether KA exerts anti-AILI effects via the Nrf2 signaling pathway. Mice were fasted for 22 h and injected intraperitoneally with APAP (250 mg kg−1) to induce AILI. Mice were pre-injected intragastrically with KA for 2 h followed by APAP injection. The hepatic injury was observed by H&E staining. Biochemical parameters of the serum and liver were measured using kits. KA alleviated hepatic injury and inflammatory response in AILI mice and ameliorated APAP-induced hepatic iron overload and oxidative stress in mice. In addition, the protective effects of KA against APAP-induced hepatotoxicity were examined in L02 cells in vitro. Cell viability was assayed by the CCK8 assay. Mitochondrial reactive oxygen species (ROS) in L02 cells were detected by MitoSox fluorescence. KA reversed the APAP-induced decrease in cell viability and GSH levels and inhibited the accumulation of intracellular ROS. Furthermore, KA activated the Nrf2 pathway and upregulated Gpx4 in mouse livers and L02 cells to inhibit ferroptosis induced by APAP. Finally, molecular docking indicated the potential interaction of KA with Keap1. Taken together, KA ameliorated oxidative stress and ferroptosis-mediated AILI by activating Nrf2 signaling.
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JOURNAL OF CONTROLLED RELEASE
·
2022
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IF 11.467
Jianing Zhao,Longbing Ling,Wei Zhu,Tianhao Ying,Tao Yu,Mengmeng Sun,Xuan Zhu,Yuan Du,Leiming Zhang
Atherosclerosis (AS), a leading cause of death worldwide, involves chronic macrophage inflammation from its initiation to the emergence of complications. Targeting plaque inflammation by re-polarizing pro-inflammatory M1 to anti-inflammatory M2 could therefore provide a promising strategy to treat AS, but currently available anti-inflammatory drugs limit clinical outcomes. In this study, we found that kaempferol (KPF) is capable of potential anti-inflammation as a novel drug candidate, which has been scarcely reported. Building upon these findings, we fabricated a macrophage-biomimetic KPF delivery platform, abbreviated as [email protected] to potentiate therapeutic payloads, wherein the designed ROS-responsive Dextran- g -PBMEO NPs with π-π stacking were coated with macrophage membrane (MM) for effective target and accumulation in atherosclerotic lesions. Therapy of [email protected] afforded significant decrease in proliferating macrophage inflammation while went with the reduction of key pro-inflammatory cytokines and re-polarization M1 to M2 phenotype, inducing excellent anti-AS responses in ApoE −/− mice after i.p. delivery. The mechanism of [email protected] was further investigated and found it related to block the ROS/NF-κB signaling pathways. Together with as well demonstrated biosafety profiles, this proof-of-concept opens an instructive door for the study of KPF-mediated nanodrugs in treatment of AS based on biomimetic NPs.
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NAUNYN-SCHMIEDEBERGS ARCHIVES OF PHARMACOLOGY
·
2025
·
IF 3.1
Liu Wencheng,Liu Rifu,Yang Yue,Cheng Lixue,Feng Xiaobing,Li Qinglei
This study investigated the potential therapeutic effect of kaempferol on osteoporosis by regulating bone homeostasis through the YAP. The ovariectomy model was constructed. The changes in bone and liver tissue were observed through HE staining. Bone metabolism and inflammatory markers were quantitatively analyzed using RT-qPCR and ELISA. Changes in the YAP/NF-κB signaling pathway were detected through Western blot and immunofluorescence. In vitro, the activity and secretion levels of MC3 T3-E1-differentiated osteoblasts were assessed using CCK- 8 and ELISA. The effects of osteoblast-secreted factors on osteoclast-induced differentiation were analyzed using alizarin red staining, phalloidin staining, ELISA, TRAP staining, and SEM. Finally, the regulatory effects of kaempferol on the expression of bone homeostasis in osteoclasts were examined by immunofluorescence and Western blot. Kaempferol treatment improved trabecular bone structure, increased bone density, and modulated bone metabolism by enhancing OPG expression and suppressing TRAP, NFATC1, and RANKL levels. Kaempferol inhibited the activation of the NF-κB pathway and increased YAP expression, reducing inflammatory factors. In vitro, kaempferol promoted osteoblast differentiation and inhibited osteoclast activity. These effects were most pronounced at higher kaempferol doses and were associated with improved bone remodeling and reduced bone resorption. Kaempferol exhibits significant potential for osteoporosis treatment by regulating bone homeostasis, mitigating inflammation through modulating the YAP.
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NEUROREPORT
·
2025
·
IF 1.7
Zhou Shinan,Liang Lu,Zhong Wenyan,Chen Jingjing,Xiao Li
Excessive neuroinflammation resulting from chronic alcohol intake is an important risk factor for central nervous system injury. The aim of this study was to investigate the effect of kaempferol (KAE) on alcohol-induced neural injury and its underlying mechanism. C57BL/6 N mice were employed to develop a binge-on-chronic alcohol exposure model, with different doses of KAE as an interventional drug for 6 weeks. Neuronal damage and microglial activation in the brain, as well as colonic tissue damage and serum lipopolysaccharide (LPS) concentrations, were systematically assessed. Additionally, Caco-2 cells were exposed to alcohol to induce intestinal epithelial injury in vitro. Chronic alcohol exposure let to significant neuronal damage in the cortex and hippocampus of mice. KAE treatment effectively attenuated microglial activation and reduced neuronal damage in the brains of alcohol-exposed mice. Analysis of colonic tissues revealed that KAE administration inhibited miRNA-122a expression, alleviated pathological damage, and enhanced occludin expression, thereby significantly lowing serum LPS concentrations in alcohol-fed mice. In vitro, KAE markedly decreased miRNA-122a expression and enhanced occludin levels in Caco-2 cells treated with alcohol. Furthermore, overexpression of miRNA-122a was found to diminish occludin protein production in Caco-2 cells, which was significantly counteracted by KAE treatment. KAE treatment enhanced intestinal barrier function to alleviate neuronal damage caused by microglial activation mediated by gut-derived LPS under alcohol expose. This effect of KAE was involved in the enhance of intestinal occludin expression by inhibiting the expression of miRNA-122a. This suggested that KAE had the potential to prevent alcohol-induced neurological damage.
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PHARMACOLOGY
·
2024
·
IF 2.9
Zhong Wenyan,Chen Jingjing,Xu Guangfu,Xiao Li
Introduction: To investigate the effect and mechanism of Kaempferol on alcoholic steatohepatitis. Methods: C57BL/6 N mice were utilized to establish Binge-on-Chronic alcohol exposure mice model. Kaempferol was given as the interventional drug to chronic alcohol-fed mice for six weeks to assess its effects. In vitro, intestinal epithelial Caco-2 cells were stimulated by alcohol, and miRNA-155 mimics were used to further study the effect of kaempferol to miRNA-155 signaling in intestinal epithelial cells. HE staining and oil red O staining were used to observe the liver and intestinal tissue damage in each group of mice, and ALT, AST, IL-1B and TNF-a were detected by kits; LPS expression was detected by ELISA kit, and the expression of IL-1B and TNF-a was assessed by qRT-PCR; activated inflammatory response of liver and colon tissue and the related signalling pathway activation. Results: Kaempferol treatment significantly improved pathological changes such as steatosis and vacuolated lesions in liver tissue of the alcohol diet model group, and reduced serum ALT and AST enzyme activities and liver tissue interleukin-1β and tumour necrosis factor-α mRNA expression levels. Kaempferol significantly reduced the expression of miRNA-155 in the intestinal tissue of alcohol-fed mice, significantly increased their SOCS1 protein expression, inhibited the activation of nuclear factor kappa-B and significantly increased the production of the intestinal tight junction proteins occludin and ZO-1. What's more, kaempferol significantly reduced serum LPS levels in ASH mice. In vitro experiments showed that compared with the control group, kaempferol significantly inhibited the expression level of miRNA-155 in Caco-2 cells under ethanol exposure, decreased the activation of nuclear factor kappa-B, led to an increase in the expression of SOCS1 protein, and increased the production level of occludin protein in Caco-2 cells under the effect of alcohol. In contrast, overexpression of miRNA-155 significantly decreased occludin and SOCS1 protein production and increased nuclear factor kappa-B activation levels in Caco-2 cells, and the administration of kaempferol significantly inhibited this effect. Conclusion: Kaempferol improved the stability of gut barrier function to ameliorate hepatic injury induced by alcohol intake through enhancing occludin protein expression, by targeting miR-155 to inhibit the excessive inflammatory response in the intestine
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FLUID PHASE EQUILIBRIA
·
2021
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IF 2.775
Maolin Li,Yumin Liu,Mengya Li,Zeren Shang,Mingdi Liu,Dandan Han
The solubility of kaempferol monohydrate (KFM) in five mono-solvents (ethanol, 1-propanol, 2-propanol, 1-butanol, 2-butanol) and three binary solvents (ethanol + water, 1-propanol + water, 2-propanol + water) was measured by gravimetric method from 283.15 K to 323.15 K at the pressure of 0.1 MPa. It is concluded that solubility of KFM is a function of temperature and solvent composition. Statistical method was used to analyze the impact of physicochemical parameters of solvents on solubility of KFM, indicating that comprehensive factors, such as the hydrogen bonding donor capacity and cohesive energy density would influence on solubility of KFM. In addition, the COSMO-RS model was used to explore the effects of solvent-solute interactions on solubility of KFM. Further, the solubility data was correlated by the modified Apelblat equation, λh equation, and van't Hoff equation, in which the modified Apelblat equation showed the best correlation result. In the final, the apparent thermodynamic properties ( Δ sol H 0 , Δ sol G 0 , Δ sol S 0 ) of KFM were derived through the van't Hoff equation, demonstrating the dissolution process of KFM in the selected solvents was endothermic. We hope the solubility of KFM determined in this work provides data can support for its further purification.
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JOURNAL OF ALLOYS AND COMPOUNDS
·
2026
·
IF 6.3
Jing Chen,Wenjing Liu,Rongfang Ma,Jingjing Nan,Shuai Wang
Kaempferol (KA) is an important natural flavonoid compound, and its sensitive detection is of great significance in food science and pharmacological analysis. To address the problems of traditional electrochemical sensors being susceptible to environmental interference and having poor stability in complex samples, this study successfully prepared a polydopamine-modified MXene/methylene blue composite material (PDA@MXene/MB), and constructed a novel ratio electrochemical sensor for the highly selective and sensitive detection of kaempferol. This sensor utilizes the high conductivity and large specific surface area of MXene as an ideal base, and through the in-situ polymerization of polydopamine, effectively prevents the stacking of MXene layers and simultaneously fixes methylene blue (MB) as a stable and reliable internal reference signal. During the detection process, the ratio of I KA /I MB is used for quantitative analysis, effectively eliminating the interference of background current fluctuations and environmental factors. Experimental results show that this sensor exhibits excellent analytical performance for kaempferol, presenting a good linear relationship within the concentration range of 0.4-36 µM, with a detection limit of 49 nM. Moreover, the sensor demonstrates good selectivity, reproducibility and stability, and it was also successfully used to determine kaempferol in actual tablet sample, yielding satisfactory recovery rates.
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Translational Cancer Research
·
2026
·Vol. 15
·期 3
·179
·
IF 2.1
Jia-Yi Lu,Xin-Miao Zhao,Xian-Bao Liu,Li Gao
Background Oral squamous cell carcinoma (OSCC) is the most common oral malignancy, affecting the tongue, palate, mouth floor, alveolar ridge, and buccal mucosa. Kaempferol, a natural flavonoid, exhibits anti-oral cancer properties, but its mechanisms remain unclear. This study aimed to investigate kaempferol’s therapeutic potential and molecular mechanisms in OSCC using network pharmacology, molecular docking, and experimental validation. Methods Kaempferol’s components and targets were identified via the Traditional Chinese Medicine Systems Pharmacology Database and Analysis Platform (TCMSP). OSCC-related genes were sourced from GeneCards and Gene Expression Omnibus (GEO) databases. Network and molecular docking analyses were performed using Cytoscape and Autodock, respectively. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses were conducted using Database for Annotation, Visualization and Integrated Discovery (DAVID). In vitro and in vivo experiments validated kaempferol’s effects. Results Kaempferol induced ferroptosis, reducing OSCC cell viability and increasing apoptosis dose-dependently. Carbonic anhydrase IX (CA9) emerged as a core gene mediating kaempferol’s anti-OSCC effects via ferroptosis. Molecular docking confirmed strong binding affinity between kaempferol and CA9 (−6.24 kcal/mol). GO and KEGG analyses revealed kaempferol’s modulation of p53/FoxO/cellular senescence pathways. Experiments confirmed kaempferol’s inhibition of OSCC proliferation and migration through CA9/ferroptosis induction. Conclusions Kaempferol exerts anti-OSCC effects via CA9/ferroptosis, highlighting its potential as a therapeutic agent for OSCC.
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PHYTOTHERAPY RESEARCH
·
2022
·Vol. 36
·期 4
·1678-1691
·
IF 6.388
Shiquan Chang,Xin Li,Yachun Zheng,Huimei Shi,Di Zhang,Bei Jing,Zhenni Chen,Guoqiang Qian,Guoping Zhao
Switching microglial polarization from the M1 to M2 phenotype is a promising therapeutic strategy for neuropathic pain (NP). Toll-like receptor 4 (TLR4) is activated by lipopolysaccharide (LPS). Uncontrolled activation of TLR4 has been proven to trigger chronic inflammation. Kaempferol, a dietary flavonoid, is known to have anti-inflammatory properties. This study is aimed to investigate the analgesic and anti-inflammatory effects and the underlying mechanisms of kaempferol, which were explored with an NP model in vivo and LPS-induced injury in microglial BV2 cells in vitro. The levels of proinflammatory cytokines were evaluated. H&E staining and immunohistochemistry were used to assess the sciatic nerve condition after chronic constriction injury surgery. Western blotting and immunofluorescence were used to determine whether TLR4/NF-ĸB signaling pathway plays a major role in kaempferol-mediated alleviation of neuroinflammation. Quantitative real-time polymerase chain reaction and flow cytometry were used to examine the modulator effect of kaempferol on microglial M1/M2 polarization. We found that kaempferol treatment can significantly reduce NP and proinflammatory cytokine production. Kaempferol attenuated the activation of TLR4/NF-κB pathways in LPS-activated BV2 cells. The analgesic effects of kaempferol on NP may be due to inhibition of microglia activation and switching the M1 to M2 phenotype.
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SPECTROCHIMICA ACTA PART A-MOLECULAR AND BIOMOLECULAR SPECTROSCOPY
·
2020
·
IF 3.232
Lu Sun,Xiaoqing Wang,Jiuzhou Shi,Shilong Yang,Li Xu
In this work, a natural product probe, kaempferol, which exhibited aggregation-induced emission (AIE) characteristic in water/tetrahydrofuran (THF) binary solvent was explored. The probe showed high resistance to photobleaching capacity and excellent selectivity towards Al 3+ in the aggregation state. Upon the addition of Al 3+ , the probe displayed more than 12-fold (I 486 /I 421 ) fluorescence intensity enhancement, accompanied by a color change, suggesting that the aggregated kaempferol can be used as a ratiometric probe for Al 3+ detecting. Notably, promising selectivity to Al 3+ within the pH range of 6–8 made the probe suitable for physiological conditions. Further Arabidopsis thaliana root imaging experiment demonstrated that the probe could image Al 3+ in the plant.
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JOURNAL OF PHARMACOLOGY AND EXPERIMENTAL THERAPEUTICS
·
2025
·
IF 3.8
Jiajia Chen,Huanle Liu,Yanfang Fu,Xiaolan Chen,Shiqin Zhang,Yongqi Yang,Shengwen Li,Guixiang Wang,Tian Lan
Background Chronic liver inflammation is a major cause of death in patients with liver fibrosis and cirrhosis, which pose a serious health threat worldwide, and there is no effective anti-hepatic fibrosis drug. Kaempferol (KA), a flavonoid polyphenol extracted from many edible plants and traditional Chinese medicine, has been reported to possess anti-inflammatory, antioxidant, and antitumor activities and has an ameliorating effect on liver fibrosis or other fibroproliferative diseases. However, the specific regulatory mechanism of KA-reversed macrophage M1 polarization is still obscure. This study aimed to investigate the protective effects of KA on carbon tetrachloride (CCl 4 )-induced liver fibrosis in mice through M1 polarization. Methods C57BL/6 mice were intraperitoneally injected with CCl 4 twice weekly to induce liver fibrosis. Male mice were randomly divided into four groups (n = 5): the oil group, the CCl 4 group, the low-dose KA-treatment CCl 4 group (50 mg/kg/d KA), and the high-dose KA-treatment CCl 4 group (100 mg/kg/d KA). An equal amount of solvent was given to each group by intraperitoneal injection. Results The results indicated that KA decreased liver pathologic changes, hepatic macrophage recruitment, and serum alanine aminotransferase (ALT) levels. Notably, it reduced the activation of M1-type macrophages in the liver. The expression of proinflammatory cytokines and genes associated with M1 macrophages, such as tumor necrosis factor-alpha (TNF-α), interleukin-6 (IL-6), IL-1β, and inducible nitric oxide synthase (iNOS), was also decreased. The core targets, signaling pathways, and possible mechanisms related to the M1 polarization of KA were analyzed by network pharmacology and molecular docking. Further analysis revealed that KA regulated MAPK/NF-κB signaling pathways. Finally, the results indicated that KA regulates M1 macrophage activation by modulating the MAPK/NF-κB signaling pathways. Conclusions This study revealed that KA ameliorated liver injury, inflammation, and fibrosis by inhibiting macrophage M1 polarization through the MAPK/NF-ҡB signaling pathway, highlighting KA as a potential novel agent for the prevention and treatment of liver fibrosis.
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