RSC Advances
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2018
·Vol. 8
·期 43
·24470-24476
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IF 2.936
Xiaofang Chen,Jianyang Tan,Lu Zhang,Yonggang Liu,Yahong Cheng,Qianying Zhang,Hong Ding
The abuse of fructose in daily diet may cause cardiovascular diseases that seriously threaten human health, and both safe and efficient solutions need to be developed. We investigated whether apigenin can prevent the harmful impact of excessive fructose on cardiovascular events. Based on the reduction of percentage of body fat and systolic pressure as well as the improvements in insulin resistance, lipid metabolism, and pathological injury to the thoracic aorta, we suggested that high levels of fructose cause vascular injury and metabolic disorders, which can be improved to some extent by using apigenin. Fundamentally, apigenin down-regulates levels of phosphoinositide 3-kinase (PI3K), protein kinase B (AKT), and glucose transporter 1 (GLUT1), which increase with high concentrations of fructose. Moreover, the inflammation and asymmetric dimethylarginine (ADMA) levels increased in fructose group, but they decreased when the rats were fed with apigenin. The results suggest that PI3K/AKT/GLUT1 may have potential for alleviating cardiovascular injury, and apigenin can be an excellent candidate for supplements to ameliorate cardiovascular diseases related to high fructose consumption.
研究领域:
药理学
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心血管疾病
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代谢
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营养学
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DOI
PubMed
高影响因子
REACTIVE & FUNCTIONAL POLYMERS
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2021
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IF 3.975
Wenmei Tan,Wei Shi,Sheng Ding,Zhengfeng Xie
Using renewable substances as the raw materials, and through relatively greener synthetic processes to implement the preparation of novel functional polymers is an idea that accords with the concept of “sustainable development” and is highly desirable in nowadays polymer science. In this study, apigenin (as renewable phenol) and furfurylamine (as renewable amine) were selected to prepare bio-based benzoxazine derivative (AP-f) through Mannich reaction . Using AP-f and diphenylmethane-based diisocyanide (IC) as reactants, a type of cross-linked, semi-aromatic polyamide derivative (Bio-PA) was successfully prepared via benzoxazine-isocyanide mechanochemistry (BIC-MC) by ball milling manner. Chemical structure , elemental composition , micro morphology and stacking state properties of Bio-PA were systematically characterized here. Multiple Pb(II)-affinitive molecular fragments (phenolic hydroxyl , tertiary amine and amide) were integrated into the structure of Bio-PA. Based on this, the application of Bio-PA as “enrichment-type” Pb(II) electrochemical probe was explored subsequently. The results showed that the introduction of Bio-PA significantly improved the response of Pb(II), and the modified electrode (Bio-PA/Nafion/GCE) illustrated satisfactory detection sensitivity and selectivity.
研究领域:
聚合物科学
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可持续化学
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环境化学
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电化学
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高影响因子
SPECTROCHIMICA ACTA PART A-MOLECULAR AND BIOMOLECULAR SPECTROSCOPY
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2022
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IF 4.831
Jinying Guo,Chuanfa Gan,Bo Cheng,Bo Cui,Fankai Yi
Pepsin plays an important role in nutrient metabolism. Apigenin (AP) is a beneficial polyphenol to human health. To enhance the bioavailability of AP and elucidate the inhibitory effect of AP on pepsin, the interaction mechanism of AP with pepsin was investigated using spectroscopic analysis and molecular docking, and the activity of pepsin and antioxidant activity of AP was also evaluated. Specifically, AP performed static quenching of pepsin and had only one binding site on pepsin. More interestingly, the interaction between AP and pepsin was spontaneous, while hydrogen bonds and van der Waals forces were the main binding forces. Generally, synchronous and three-dimensional fluorescence confirmed that AP induced the conformational changes of pepsin, and molecular docking proved the above results and illustrated the specific binding patterns. Specifically, AP inhibited the activity of pepsin, while pepsin decreased the antioxidant activity of AP. These results provided useful information for elucidating the interactions between AP and pepsin.
研究领域:
生物化学
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营养学
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药物化学
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DOI
PubMed
高影响因子
Journal of Functional Foods
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2023
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IF 5.6
Yeye Hu,Xueting Guan,Ziliang He,Yuan Xie,Zhiqiang Niu,Wei Zhang,Aoran Wang,Ji Zhang,Chuanling Si,Fu Li,Weicheng Hu
Apigenin-7-O-glucoside (AG), a flavonoid glycoside, has been shown in vitro anti-inflammatory activities. To date, the mechanism of AG against colitis has not been reported. In this study, we investigated the role of AG in relieving colitis and explored its potential mechanisms in dextran sulfate sodium (DSS)-induced colitis mice. The results indicated oral administration of AG increased colon length and improved colonic histopathology. Besides, it dramatically restored the colonic expression of pro-inflammatory and anti-inflammatory mediators, as well as enhanced the expression of intestinal barrier markers such as ZO-1, occludin, claudin-1, and claudin-3. The mitogen-activated protein kinases (MAPKs) including ERK, JNK, and p38 were significantly inhibited. Moreover, 16S rDNA sequencing revealed that AG improved the abundance of Akkermansia , and reduced that of Bacteroides and Desulfovibrio . Taken together, AG supplementation relieved DSS-induced colitis by protecting the intestinal barrier, inhibiting the MAPK pathway, and modulating gut microbiota, which indicated that AG may be a good candidate therapeutic compound for sustaining gut health to lower the risk of colitis.
研究领域:
药理学
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免疫学
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胃肠病学
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微生物学
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DOI
高影响因子
FISH & SHELLFISH IMMUNOLOGY
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2025
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IF 3.9
Tianyue Guan,Wenjing Zhou,Yaxin Gao,Qian Dong,Xiaomin Jin,Yusa Li,Zihan Xu,Hong Yu,Jingquan Dong
The triazole fungicide difenoconazole (DFZ) is widely used in agriculture and frequently detected in aquatic environments, posing potential risks to non-target organisms despite its regulatory classification as low toxicity. This study investigated the protective effects of apigenin (API), a natural flavonoid, against DFZ-induced multi-organ toxicity in carp ( Cyprinus carpio ). Fish were exposed to DFZ (0.3906 mg/kg body weight) alone or in combination with dietary API (50 mg/kg feed) for 30 days. Chronic DFZ exposure induced severe histopathological lesions in the heart, kidney, and intestine, increased serum cardiac injury markers (CK and CK-MB), disrupted redox homeostasis—evidenced by elevated ROS and MDA and reduced CAT, GSH, and T-AOC—and upregulated pro-inflammatory cytokine mRNA ( tnf-α , il-1β , il-6 , inos ). At the protein/transcriptional level, DFZ increased iNOS while decreasing Nrf2/HO-1, and suppressed antioxidant genes ( cat , sod , gpx ). Apigenin supplementation significantly attenuated tissue damage, restored antioxidant capacity, suppressed inflammatory responses while promoting il-10 , normalized iNOS and Nrf2/HO-1, up-regulated cat/sod/gpx, and alleviated DFZ-induced impairment of growth performance. These results demonstrate that apigenin alleviates DFZ-induced cardiorenal and intestinal injury by modulating oxidative stress and inflammation. Our findings highlight the potential of apigenin as a dietary protective agent against environmental fungicide toxicity in aquatic species.
研究领域:
毒理学
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水生生态学
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环境科学
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鱼类生理学
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分子生物学
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DOI
PubMed
高影响因子
Thoracic Cancer
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2026
·Vol. 17
·期 17
·e70383
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IF 2.6
Kairui Zhu,Yulong Mu,Zhenguo Su,Zhen Yue,Dongyang Wu,Guiwu Qu,Chenyang Jiang,Qing Li,Youjie Li,Ning Xie
Background Pyroptosis-related signaling contributes to lung adenocarcinoma (LUAD) progression and prognosis. Apigenin (AP) has anti-inflammatory and cytoprotective properties, but its effects on pyroptosis-associated signaling in injured LUAD cells remain unclear. Methods A549 cells were treated with carbonyl cyanide m -chlorophenyl hydrazone (CCCP) and ferrous sulfate (FeSO 4 ) to establish a cellular injury model. Cell morphology, Cell Counting Kit-8 signals, and pyroptosis-associated proteins were assessed after AP treatment. Network pharmacology, molecular docking, molecular dynamics simulations, and analyses of The Cancer Genome Atlas and Gene Expression Omnibus datasets were used to prioritize candidate targets, characterize pyroptosis-related genes, and develop a prognostic signature. Results CCCP/FeSO 4 reduced CCK-8 signals and induced morphological injury, whereas AP partially reversed these changes. AP also reduced alterations in GSDMD-N, caspase-1, IL-1β, TNF-α/NF-κB pathway proteins, AIM2, and ASC. TNF was prioritized as a candidate target, and computational analyses predicted a potentially stable AP–TNF interaction without demonstrating direct binding. Bioinformatic analyses identified distinct pyroptosis-related LUAD subgroups and generated a prognostic signature that stratified survival in training and external validation cohorts. AIM2 was additionally prioritized as a LUAD- and stress-associated candidate. Conclusion AP attenuated CCCP/FeSO 4 -induced injury and pyroptosis-associated molecular changes in A549 cells, potentially through TNF-α/NF-κB and AIM2-related signaling. Further mechanistic validation is required.
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Asian Journal of Pharmaceutical Sciences
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2025
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IF 11.9
Wei-Ran Cao,Xue Zhang,Jia-Xuan Chen,Lu Sun,Hui-Ning He,Fei Yu
Mitochondria provides adenosine triphosphate for multiple vital movements to ensure tumor cell proliferation. Compared to the broadly used method of inducing DNA replication arrest to kill cancer, inducing mitochondria damage to cause energy shortage is quite promising as it can inhibit tumor cell bioactivities, increase intracellular accumulation of toxic drugs, eventually sensitize chemotherapy and even reverse drug resistance. Breaking the balance of glutathione (GSH) and reactive oxygen species (ROS) contents have been proven efficient in destroying mitochondria respectively. Herein, apigenin, a GSH efflux reagent, and 2′-deoxy-5-fluorouridine 5′-monophosphate sodium salt (FdUMP) that could induce toxic ROS were co-delivered by constructed lipid nanoparticles, noted as Lip@AF. An immune-checkpoint inhibition reagent CD276 antibody was modified onto the surface of Lip@AF with high reaction specificity (noted as αCD276-Lip@AF) to enhance the recognition of immune cells to tumor. Results showed that the redox balance was destroyed, leading to severe injury to mitochondria and cell membrane. Furthermore, synergistic DNA/RNA replication inhibition caused by inhibiting the function of thymidylate synthase were observed. Eventually, significantly enhanced cytotoxicity was achieved by combining multiple mechanisms including ferroptosis, apoptosis and pyroptosis. In vivo , strengthen tumor growth inhibition was achieved by αCD276-Lip@AF with high biosafety, providing new sights in enhancing chemotherapy sensitiveness and achieving high-performance chemo-immunotherapy.
研究领域:
肿瘤学
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药理学
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免疫学
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产品关联
DOI
PubMed
高影响因子
BIOORGANIC CHEMISTRY
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2024
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IF 4.5
Honghui Liu,Yanxu Wei,Yan Wang,Qiu Zhao,Lan Liu,Hong Ding,Yuntian Hong
Due to the high incidence of diabetes and its associated complications, diabetes is widely recognized as a serious global health problem. In diabetes treatment strategies, targeting α-glucosidase, a key carbohydratehydrolyzing enzyme, has emerged as a highly regarded approach. To develop novel α-glucosidase inhibitors, we successfully synthesized a series of apigenin analogs, collectively referred to as H1 – H27 compounds and examined their inhibitory effects on α-glucosidase activity. H7 showed a remarkable inhibitory effect, surpassing that of the standard drug acarbose. Further analysis revealed that H7 , H10 , and H24 act as non-competitive inhibitors of α- glucosidase. In vivo experiments using a type 2 diabetes mouse model demonstrated the diverse therapeutic potential of H7 ; it effectively lowered blood sugar levels, improved glucose tolerance, and corrected lipid metabolism. In addition, H7 showed hepatoprotective effects, highlighting its ability to improve liver function. H7 also positively influenced the gut microbiota composition in diabetic mice, increasing diversity and richness. These results highlight the promising therapeutic effects of apigenin analogs, such as H7 , for treating type 2 diabetes and show how they could provide numerous benefits, including effective inhibition of α-glucosidase, improved glucose control, correction of lipid metabolism, hepatoprotection, and modulation of the intestinal microbiota.
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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代谢研究
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微生物组研究
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DOI
PubMed
高影响因子
EUROPEAN JOURNAL OF PHARMACOLOGY
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2020
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IF 3.263
Fei-fei Pan,Yan-Biao Zheng,Chuan-Jian Shi,Feng-wei Zhang,Jin-fang Zhang,Wei-ming Fu
Hepatocellular Carcinoma (HCC) is one of the leading causes of cancer-related deaths in the world. However, the effective pharmacological approaches remain scanty in clinical practice. As a bioactive flavonoid , apigenin (API) is enriched in common fruits and vegetables. Although pharmacological activities of API have been widely investigated, its biological function in HCC remains obscure. In the present study, we found that API strongly suppressed cell growth and induced apoptosis in HCC cells. Using a xenograft mice model, API was demonstrated to inhibit the in vivo tumor growth. It is known that the long non-coding RNA H19, which is frequently elevated in HCC, plays a vital role in mediating tumorigenesis and cancer progression. Our results demonstrated that H19 was down-regulated by API, and thereby induced the inactivation of the canonical Wnt/β-catenin signaling. In conclusion, our results demonstrated that API was able to suppress tumor growth of HCC through H19-mediated Wnt/β-catenin signaling regulatory axis, suggesting that API may be a promising candidate for developing novel therapeutic approaches against liver cancer.
研究领域:
肿瘤学
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分子生物学
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药理学
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DOI
PubMed
高影响因子
JOURNAL OF MOLECULAR LIQUIDS
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2021
·
IF 6.165
Sha Li,Xing Hu,Junhui Pan,Deming Gong,Guowen Zhang
The inhibition of pancreatic lipase by apigenin, a natural dietary flavonoid, was investigated by various spectroscopic techniques and computational simulation. The results showed that apigenin reversibly inhibited pancreatic lipase activity in a competitive manner with an IC 50 value of 0.45 ± 0.03 mM, and its combination with orlistat showed a synergistic effect. Formation of a complex between apigenin and pancreatic lipase driven by hydrogen bonds resulted in the fluorescence quenching of the enzyme through a static manner. The binding constant of apigenin with the enzyme was (5.47 ± 0.01) × 10 4 L mol −1 at 298 K, and the kinetic process of their interaction was characterized by the resolved concentration profiles and pure spectra of different components from the multivariate curve resolution-alternating least squares algorithm. The inhibition of pancreatic lipase by apigenin was mainly attributed to the tighter structure of the enzyme and the interaction between apigenin and the amino acid residues in the active center of the enzyme to prevent the substrate from being oxidized, as demonstrated by the analysis of circular dichroism spectra and molecular docking. Molecular dynamics simulation further characterized the binding conformation and property of apigenin-pancreatic lipase complex. This study provides novel insights into the mechanism of apigenin as pancreatic lipase inhibitor and the development of apigenin as an anti-obesity nutrient.
研究领域:
药理学
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生物化学
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分子生物学
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营养学
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高影响因子
CLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY
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2014
·Vol. 42
·期 2
·146-153
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IF 2.405
Xiao-Yun Hu,Ji-Yun Liang,Xue-Jun Guo,Li Liu,Ya-Bing Guo
Summary The development of chemoresistance may reduce the efficacy of chemotherapeutic drugs for treating hepatocellular carcinoma (HCC). In the present study, the effects of apigenin on intensifying the chemosensitivity of HCC cells and an HCC xenograft model in response to 5-fluorouracil (5-FU) were investigated. Sub-toxic concentrations of apigenin (4 μ mol/L) significantly enhanced the cytotoxicity of 5-FU (100 μ g/mL) in HCC cells. In vivo , combined treatment with apigenin (20 mg/kg, five times/week for 3 weeks) and 5-FU (20 mg/kg for 5 consecutive days) significantly inhibited the growth of HCC xenograft tumours. Annexin V–propidium iodide dual staining assays, terminal deoxyribonucleotidyl transferase-mediated dUTP–digoxigenin nick end-labelling assays and western blotting analysis were used to confirm the synergistic effects of apigenin and 5-FU on HCC apoptosis. Coincubation of HCC cells with apigenin and 5-FU increased levels of reactive oxygen species (ROS), which was followed by a decrease in the mitochondrial membrane potential (ΔΨm). In addition, combined triggered the mitochondrial apoptotic pathway, as indicated by decreased Bcl-2 expression and loss of ΔΨm, with significant activation of caspase 3 and poly(ADP-ribose) polymerase. The present study is the first to demonstrate that apigenin may potentiate the cytotoxicity of 5-FU in HCC via inhibition of ROS-mediated drug resistance and concurrent activation of the mitochondrial pathways of apoptosis.
研究领域:
肿瘤学
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药理学
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细胞生物学
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DOI
PubMed
高影响因子
Food Bioscience
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2021
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IF 4.24
Fuqiang Liang,Yumeng Shi,Weiwei Cao,Jiayi Shi
This study aimed to elucidate the inhibition mechanism of apigenin against porcine pancreatic lipase (PPL), and, moreover, to comprehensively reveal the molecular basis of its anti-obesity via network pharmacology approach. The results showed that apigenin inhibited PPL with an IC 50 value of 0.377 ± 0.041 mM. Spectroscopic techniques combined molecular docking suggested that apigenin could bind into the PPL active pocket, affecting its normal spatial conformation. Moreover, molecular dynamic (MD) simulations revealed that the open conformation of PPL tended to transit to the closed in the presence of apigenin, which might one important reason for the inhibition of PPL catalytic ability. Network pharmacology analysis revealed that a total of 49 proteins could be identified as potential targets for the anti-obesity effects of apigenin. According to the protein-protein interaction (PPI) network analysis, six hub targets were extracted including IGF1 , ESR1, MMP9 , PPARA , MAPK14 and NR3C1. Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment indicated that the 49 potential targets could be mapped to 30 pathways (p<0.05). Among them, PI3K-Akt signaling pathway and insulin resistance can be considered as two major pathways regulated by apigenin. Further docking studies indicated that apigenin can bind into the binding pocket of the six hub target proteins identified according to the PPI network. The results indicated that in addition to inhibiting PPL, apigenin could exhibit anti-obesity benefit through the molecular mechanisms uncovered by network pharmacology. This study proposes a new strategy to reveal the mechanisms of dietary polyphenols at the level of network pharmacology.
研究领域:
药理学
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分子生物学
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生物信息学
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高影响因子
危险品化学品经营许可证（带存储）