FLUID PHASE EQUILIBRIA
·
2021
·
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.
研究领域:
化学工程
·
药学
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DOI
高影响因子
Advanced Healthcare Materials
·
2026
·
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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PubMed
高影响因子
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.
研究领域:
药理学
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骨生物学
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信号通路研究
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DOI
PubMed
高影响因子
PLoS One
·
2025
·Vol. 20
·期 6
·e0325189
·
IF 2.6
Yu Wang,Chaofan Chen,Yushan Li,Ran Li,Jinghan Wang,Chao Wu,Haonan Chen,Yingchao Shi,Shengfang Wang,Chuanyu Gao
Kaempferol exhibits various biological activities, including antioxidant and anti-inflammatory effects. Its role in modulating lipid metabolism and inhibiting inflammatory responses to suppress the progression of atherosclerosis has been confirmed. However, its impact on macrophage pyroptosis and the underlying mechanisms remain unclear. This study aims to investigate the effects of kaempferol (Kae) on lipopolysaccharide (LPS)-induced macrophage pyroptosis and its potential mechanisms. In the experiments, we used the CCK8 assay to evaluate cell viability, ROS detection kits to measure intracellular reactive oxygen species (ROS) levels, Western Blot to detect the expression of proteins such as NOD-like receptor family pyrin domain-containing 3 (NLRP3), nuclear factor erythroid 2-related factor 2 (NRF2), gasdermin D (GSDMD), and heme oxygenase-1 (HO-1), and immunofluorescence to observe NRF2 nuclear translocation. The results showed that kaempferol alleviated LPS-induced cell viability decline and lactate dehydrogenase (LDH) release, inhibited excessive ROS generation, and suppressed NLRP3 inflammasome activation by increasing glutathione (GSH) and HO-1 levels, thereby reducing the expression of inflammatory factors. Additionally, kaempferol promoted NRF2 nuclear translocation, and the application of the NRF2 inhibitor ML385 reversed its antioxidant and anti-inflammatory effects. In vivo experiments further confirmed that kaempferol inhibited oxidative stress and reduced macrophage pyroptosis by activating the NRF2 pathway.
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PubMed
高影响因子
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.
研究领域:
神经科学
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药理学
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分子生物学
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PubMed
高影响因子
FOOD RESEARCH INTERNATIONAL
·
2026
·
IF 8
Mengli Geng,Dandan Ma,Zhaojun Wang,Qiuming Chen,Maomao Zeng,Jie Chen,Benu Adhikari,Hongyang Pan,Zhiyong He
Kaempferol (KAE) is a dietary flavonoid with recognized effects on glucolipid metabolism and oxidative stress, but its poor lipophilicity and low bioavailability limit its application. In this study, KAE derivatives with different fatty acid chain lengths (C2–C12) were synthesized using acylation catalyzed by lipozyme TL IM, and their biological activities were then systematically evaluated. In vivo assays in hyperglycemic zebrafish ( Danio rerio ) demonstrated that two medium-chain derivatives, 4’- O -octanoyl-kaempferol (C8-KAE) and 4’- O -decanoyl-kaempferol (C10-KAE), exerted superior effects on glucose regulation, lipid metabolism, and oxidative stress compared with KAE. RT–qPCR analysis showed that C8-KAE and C10-KAE more effectively coordinated the expression of key genes governing gluconeogenesis, glycogen synthesis, lipogenesis, and fatty acid oxidation, indicating multi-target regulation of glucolipid homeostasis. Subsequent in vitro tests confirmed their stronger α-glucosidase inhibitory activity than KAE, while molecular docking, molecular dynamics simulations, and MM/GBSA binding free energy analyses consistently indicated more stable and favorable binding interactions with the enzyme. These findings indicate that medium-chain acylation is an efficient strategy to upgrade KAE into more potent modulators of glucolipid metabolism and identify C8-KAE and C10-KAE as promising lead compounds.
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高影响因子
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
研究领域:
药理学
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肝病学
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胃肠病学
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分子生物学
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DOI
PubMed
高影响因子
JOURNAL OF CONTROLLED RELEASE
·
2022
·
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.
研究领域:
药理学
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纳米技术
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心血管疾病
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炎症
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药物递送系统
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DOI
PubMed
高影响因子
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.
研究领域:
药理学
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毒理学
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分子生物学
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细胞生物学
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DOI
PubMed
高影响因子
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.
研究领域:
药理学
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肝脏病学
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分子生物学
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DOI
PubMed
高影响因子
Foods
·
2024
·Vol. 13
·期 23
·3797
·
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.
研究领域:
药理学
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糖尿病研究
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分子生物学
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代谢组学
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网络药理学
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DOI
PubMed
高影响因子
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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PubMed
高影响因子
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