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Dental Materials : Official Publication... Apr 2021The aim of this in vitro study was to incorporate two anti-caries agents, Apigenin and tt-Farnesol, to resin composite and resin cement to reduce the virulence of...
OBJECTIVES
The aim of this in vitro study was to incorporate two anti-caries agents, Apigenin and tt-Farnesol, to resin composite and resin cement to reduce the virulence of Streptococcus mutans around dental restorations.
METHODS
Apigenin (Api, 5 mM) and tt-Farnesol (Far, 5 mM) were added alone, together, and combined with fluoride (F). Biofilm of S. mutans was grown on composite discs, and the dry-weight, bacterial viability, and the polysaccharides (alkali-soluble, intracellular and water-soluble) were quantified. CLSM images of the S. mutans biofilm were obtained after three years of water-storage. The effect of the additions on the physicochemical properties and the composite colorimetric parameters were also analyzed.
RESULTS
The additions did not affect bacterial viability. Api alone and combined with Far or combined with Far and F decreased the bacterial dry-weight, alkali-soluble and intracellular polysaccharides. After three years, the composites containing the additions presented a greater EPS matrix on the top of biofilm. Statistical difference was obtained for the degree of conversion; however, the maximum polymerization rate and curing kinetics were unaffected by the additions. No difference was observed for the water-soluble polysaccharides, flexural strength, and elastic modulus. Api increased the yellowness of the composites.
SIGNIFICANCE
Api, alone and combined, reduced the expression of virulence of S. mutans without jeopardizing the physicochemical properties of the composites.
Topics: Apigenin; Biofilms; Cariostatic Agents; Composite Resins; Dental Caries; Farnesol; Humans; Streptococcus mutans; Virulence
PubMed: 33422299
DOI: 10.1016/j.dental.2020.12.005 -
Advances in Clinical and Experimental... Oct 2017Flavonoids, naturally occuring derivatives of 2-phenyl-benzo-γ-pyrone, are widespread in plants as coloring substances. Apigenin (4',5,7,-trihydroxyflavone... (Review)
Review
Flavonoids, naturally occuring derivatives of 2-phenyl-benzo-γ-pyrone, are widespread in plants as coloring substances. Apigenin (4',5,7,-trihydroxyflavone (5,7-dihydroxy-2-(4-hydroxyphenyl)-4H-1-benzopyran-4-one), molecular formula C₁₅H₁₀O⁵, is a flavonoid present in many fruits and vegetables, primarily in citrus fruits, apples, parsley and celery leaves. It is also found in some medicinal plants, including chamomile flowers, thyme, oregano, peppermint, lemon balm and yarrow, as a 7-O-glycoside with anti-inflammatory and antioxidant activity. In recent years it has attracted a great deal of interest as a bioactive substance reported to have anticancer properties. According to recent literature data, apigenin is able to reduce cancer cell glucose uptake, inhibit remodeling of the extracellular matrix, inhibit cell adhesion molecules that participate in cancer progression and hinder the development of blood vessels needed by growing tumors. It is reported to protect against a wide variety of cancers. The mechanism of anticancer activity is still under investigation and further research is needed.
Topics: Antineoplastic Agents; Apigenin; Apoptosis; Cell Cycle; DNA Damage; Extracellular Matrix; Glucose Transporter Type 1; Humans; Vascular Endothelial Growth Factor A
PubMed: 29211364
DOI: 10.17219/acem/41978 -
International Journal of Molecular... May 2023Cancer is a widespread but dangerous disease that can strike anyone and is the second 1leading cause of death worldwide. Prostate cancer, in particular, is a prevalent... (Review)
Review
Cancer is a widespread but dangerous disease that can strike anyone and is the second 1leading cause of death worldwide. Prostate cancer, in particular, is a prevalent cancer that occurs in men, and much research is being done on its treatment. Although chemical drugs are effective, they have various side effects, and accordingly, anticancer drugs using natural products are emerging. To date, many natural candidates have been discovered, and new drugs are being developed as drugs to treat prostate cancer. Representative candidate compounds that have been studied to be effective in prostate cancer include apigenin, acacetin and tangeretin of the flavone family among flavonoids. In this review, we look at the effects of these three flavones on prostate cancer cells via apoptosis in vitro and in vivo. Furthermore, in addition to the existing drugs, we suggest the three flavones and their effectiveness as natural anticancer agents, a treatment model for prostate cancer.
Topics: Male; Humans; Flavones; Flavonoids; Apoptosis; Apigenin; Antineoplastic Agents; Prostatic Neoplasms
PubMed: 37298192
DOI: 10.3390/ijms24119240 -
Molecules (Basel, Switzerland) Mar 2023The overall purpose of this study was to investigate the mechanism of macrophage polarization on chondrocyte injury in osteoarthritis and the protective effect of...
OBJECTIVE
The overall purpose of this study was to investigate the mechanism of macrophage polarization on chondrocyte injury in osteoarthritis and the protective effect of apigenin on chondrocytes in osteoarthritis.
METHOD
Primary chondrocytes were isolated from the knee cartilage of three-day-old mice, and cells positive for Alsine blue staining and type II collagen immunocytochemical staining were identified and used in followup experiments. Transwell coculture was performed. Chondrocytes were inoculated in the inferior compartment, and macrophages were inoculated in the upper compartment. The experimental groups were the N group, LPS group, and LPS+ apigenin group. The effect of macrophage polarization on chondrocyte inflammation and the protective effect of apigenin on chondrocytes were verified by the drug administration. Real-time quantitative PCR (qPCR) and Western blot were used to detect the expression of RNA and protein. Experimental OA was induced by modified Hulth surgery in mice. Modified Hulth surgery was performed on the mouse's right knee to induce experimental osteoarthritis in mice, with the nonoperative right knee serving as an ipsilateral control. The mice were randomly assigned to three groups (six mice per group): the sham group, the modified Hulth group, and the modified Hulth + apigenin group. Animals were given gavage for four weeks. The protective effect of apigenin on articular cartilage was verified by histological staining and immunohistochemical analysis.
RESULTS
Histological staining showed that apigenin had a protective effect on cartilage degeneration induced by modified Hulth surgery. The PCR results showed that apigenin significantly reduced the expression levels of IL-1, IL-6, MMP3, and MMP13 in the articular cartilage of OA mice, and it had a protective effect on articular cartilage. Apigenin reduced the levels of IL-1, IL-6, TNF-α, and IL-12 in macrophages and increased the levels of MG-L1, MG-L2, ARG-1, and IL-10, which can inhibit the M1 polarization of macrophages and promote M2 polarization. In the coculture system, apigenin decreased the protein levels of TRPM7, P-mTOR, BAX, and c-caspase3 in macrophages, while significantly increasing the protein levels of Bcl2. The levels of IL-1, IL-6, MMP13, TNF-α, P38, JNK, and ERK phosphorylation were reduced in chondrocytes.
CONCLUSION
Apigenin alleviates cartilage injury in OA mice induced by modified Hulth. Apigenin inhibits chondrocyte inflammation through the MAPK pathway. Apigenin alleviates macrophage-polarization-induced inflammatory response and chondrocyte apoptosis in the macrophage-chondrocyte coculture system through the TRPM7-mTOR pathway.
Topics: Mice; Animals; Matrix Metalloproteinase 13; Apigenin; TRPM Cation Channels; Tumor Necrosis Factor-alpha; Interleukin-6; Lipopolysaccharides; Disease Models, Animal; Osteoarthritis; Inflammation; Cartilage, Articular; Chondrocytes; Macrophages; TOR Serine-Threonine Kinases; Interleukin-1
PubMed: 37049677
DOI: 10.3390/molecules28072915 -
BioMed Research International 2018The neural dysfunction is triggered by cellular and molecular events that provoke neurotoxicity and neural death. Currently, neurodegenerative diseases are increasingly... (Review)
Review
The neural dysfunction is triggered by cellular and molecular events that provoke neurotoxicity and neural death. Currently, neurodegenerative diseases are increasingly common, and available treatments are focused on relieving symptoms. Based on the above, in this review we describe the participation of vitexin in the main events involved in the neurotoxicity and cell death process, as well as the use of vitexin as a therapeutic approach to suppress or attenuate neurodegenerative progress. Vitexin contributes to increasing neuroprotective factors and pathways and counteract the targets that induce neurodegeneration, such as redox imbalance, neuroinflammation, abnormal protein aggregation, and reduction of cognitive and/or motor impairment. The results obtained provide substantial evidence to support the scientific exploration of vitexin in these pathologies, since their effects are still little explored for this direction.
Topics: Animals; Apigenin; Cell Death; Humans; Inflammation; Neurodegenerative Diseases; Neuroprotective Agents; Protein Aggregation, Pathological
PubMed: 30627560
DOI: 10.1155/2018/4785089 -
Journal of Oral Science Jul 2023Enterococcus faecalis (E. faecalis) is one of the major microorganisms that causes failure of endodontic treatment. This study aimed to investigate the antibacterial...
PURPOSE
Enterococcus faecalis (E. faecalis) is one of the major microorganisms that causes failure of endodontic treatment. This study aimed to investigate the antibacterial activity of apigenin and its synergistic effect with reduced graphene oxide (RGO) in treating E. faecalis biofilms.
METHODS
The antibacterial activities were characterized by viability analysis including colony forming units and confocal laser scanning microscopy (CLSM) analyses. The effect on biofilm biomass was measured using a crystal violet staining method. Live and dead bacteria bio-volumes were determined by CLSM analysis, and the morphology of E. faecalis biofilm after treatment with apigenin and apigenin + RGO was observed by scanning electron microscopy (SEM).
RESULTS
The viability of E. faecalis in biofilms decreased by apigenin treatment in a dose-dependent manner. While apigenin alone did not significantly affect the biofilm biomass, apigenin + RGO reduced the biomass in an apigenin concentration-dependent manner. Likewise, the bio-volume of live bacteria decreased and the bio-volume of dead bacteria increased in apigenin-treated biofilms. According to SEM images, apigenin + RGO-treated samples showed less E. faecalis in biofilms than apigenin-only treated samples.
CONCLUSION
The results suggested that the combined use of apigenin and RGO could be a potential strategy for effective endodontic disinfection.
Topics: Enterococcus faecalis; Apigenin; Biofilms; Anti-Bacterial Agents; Root Canal Irrigants
PubMed: 37211399
DOI: 10.2334/josnusd.22-0459 -
The Kaohsiung Journal of Medical... Jul 2021The present study aimed to investigate the role of apigenin and the molecular mechanism of miR-152-5p and bromodomain containing 4 (BRD4) in the proliferation, invasion,...
The present study aimed to investigate the role of apigenin and the molecular mechanism of miR-152-5p and bromodomain containing 4 (BRD4) in the proliferation, invasion, and epithelial-mesenchymal transition (EMT) of cervical carcinoma cells. Quantitative real-time PCR was used to detect the transfection efficiency and the expression of miR-152-5p and BRD4. Western blotting was conducted to evaluate the protein level of BRD4, E-cadherin, N-cadherin, and MMP9. Luciferase reporter assay was performed to confirm whether miR-152-5p bound to BRD4. MTT and Transwell invasion assay were applied to determine the cell proliferation and invasion, respectively. MiR-152-5p was downregulated and BRD4 was upregulated in cervical carcinoma tissue. Besides, miR-152-5p could directly bind to BRD4 in Hela and CaSki cells. In addition, apigenin inhibited proliferation, invasion, and EMT of Hela and CaSki cells by regulating miR-152-5p/BRD4 axis. Apigenin suppresses proliferation, invasion, and induced EMT of cervical carcinoma cells by regulation of miR-152-5p/BRD4 axis.
Topics: Apigenin; Carcinoma; Cell Cycle Proteins; Cell Line, Tumor; Cell Movement; Cell Proliferation; Epithelial-Mesenchymal Transition; Female; Gene Expression Regulation, Neoplastic; HeLa Cells; Humans; MicroRNAs; Neoplasm Invasiveness; Nuclear Proteins; Tetrazolium Salts; Thiazoles; Transcription Factors; Uterine Cervical Neoplasms
PubMed: 33611824
DOI: 10.1002/kjm2.12370 -
Scientific Reports May 2023Apigenin (APN), a flavone found in several plant foods with various biological properties such as anti-obesity, anti-inflammation and other abilities, alleviates...
Apigenin (APN), a flavone found in several plant foods with various biological properties such as anti-obesity, anti-inflammation and other abilities, alleviates atherosclerosis and non-alcoholic fatty liver disease (NAFLD) induced by a high fat diet (HFD) in mice. However, the underlying mechanisms have not been fully understood. In this study, we investigated the role of NLRP3 in anti-atherosclerosis and anti-NAFLD effect of APN in mouse models with NLRP3 deficiency. Atherosclerosis and NAFLD models were established by treatment of low density lipoprotein receptor-deficient (Ldlr) mice and NLRP3 Ldlr mice with a HFD diet (20% fat and 0.5% cholesterol) with or without APN. En face lipid accumulation analysis, plasma lipid levels, hepatic lipid accumulation and inflammation were analyzed and quantified. For in vitro experiments, HepG2 cells were stimulated by LPS plus oleic acid (OA) in the absence or presence of APN (50 μM). Lipid accumulation and the effect of APN on the NLRP3/NF-κB signaling pathway were investigated. APN administration partly reversed atherosclerosis and hepatic lipid accumulation, and decreased body weight and plasma lipid levels in Ldlr mice when fed a HFD. Compared with Ldlr mice, NLRP3 Ldlr mice showed more severe atherosclerosis and hepatic lipid accumulation. Treating the HepG2 cells with APN reduced lipid accumulation. APN also inhibited activation of the NLRP3/ NF-κB signaling pathway stimulated by OA together with LPS. Our results indicate that APN supplementation prevents atherosclerosis and NAFLD via NLRP3 inhibition in mice, and suggest that APN might be a potential therapeutic agent for the prevention of atherosclerosis and NAFLD.
Topics: Animals; Mice; Non-alcoholic Fatty Liver Disease; Inflammasomes; NLR Family, Pyrin Domain-Containing 3 Protein; Apigenin; NF-kappa B; Lipopolysaccharides; Liver; Atherosclerosis; Diet, High-Fat; Mice, Inbred C57BL
PubMed: 37198205
DOI: 10.1038/s41598-023-34654-2 -
Dental Materials Journal Dec 2020Apigenin is a type of flavonols that exhibits anti-caries properties. Bacterial adherence is the initial step in the forming of a stable biofilm that leads to caries....
Apigenin is a type of flavonols that exhibits anti-caries properties. Bacterial adherence is the initial step in the forming of a stable biofilm that leads to caries. Bacterial adherence is affected by surface characteristics, including hydrophobicity and bacterial aggregation. However, the effect of apigenin on surface characteristics of cariogenic bacteria has not been reported. We aimed to examine the effects of apigenin on adherence and biofilm formation of Streptococcus mutans UA159. Hydrophobicity and bacterial aggregation, pac and gbpC gene expressions, and cytotoxicity on human dental pulp cells were also determined. Apigenin significantly inhibited the adherence and biofilm formation of S. mutans. Hydrophobicity decreased, whereas the aggregation rate was significantly increased compared with the control. Apigenin significantly suppressed pac and gbpC gene expressions. Apigenin exhibited acceptable biocompatibility on hDPCs. Thus, apigeinin may affect adherence and biofilm formation by altering the surface properties of S. mutans without obvious adverse effect on hDPCs.
Topics: Apigenin; Biofilms; Cariostatic Agents; Dental Caries; Humans; Streptococcus mutans
PubMed: 33028784
DOI: 10.4012/dmj.2019-255 -
Translational Vision Science &... May 2020This study aims to develop an impedance-based drug screening platform that will help identify drugs that can enhance the vascular barrier function by stabilizing...
PURPOSE
This study aims to develop an impedance-based drug screening platform that will help identify drugs that can enhance the vascular barrier function by stabilizing vascular endothelial cell junctions.
METHODS
Changes in permeability of cultured human retinal microvascular endothelial cells (HRMECs) monolayer were monitored in real-time with the xCELLigence RTCA system. Using this platform, we performed a primary screen of 2100 known drugs and confirmed hits using two additional secondary permeability assays: the transwell permeability assay and the XPerT assay. The cellular and molecular mechanisms of action and in vivo therapeutic efficacy were also assessed.
RESULTS
Eleven compounds blocked interleukin 1 beta (IL-1β) induced hyperpermeability in the primary screen. Two of 11 compounds, apigenin and ethaverine hydrochloride, reproducibly blocked multiple cytokines induced hyperpermeability. In addition to HRMEC monolayers, the two compounds stabilized three other types of primary vascular endothelial cell monolayers. Preliminary mechanistic studies suggest that the two compounds stabilize the endothelium by blocking ADP-ribosylation factor 6 (ARF6) activation, which results in enhanced VE-cadherin membrane localization. The two compounds showed in vivo efficacy in an animal model of retinal permeability.
CONCLUSIONS
We developed an impedance-based cellular phenotypic drug screening platform that can identify drugs that enhance vascular barrier function. We found apigenin and ethaverine hydrochloride stabilize endothelial cell junctions and enhance the vascular barrier by blocking ARF6 activation and increasing VE-cadherin membrane localization.
TRANSLATIONAL RELEVANCE
The drugs identified from the phenotypic screen would have potential therapeutic efficacy in retinal vascular diseases regardless of the underlying mechanisms that promote vascular leak.
Topics: ADP-Ribosylation Factor 6; Animals; Apigenin; Blood-Retinal Barrier; Capillary Permeability; Endothelial Cells; Humans; Papaverine
PubMed: 32821505
DOI: 10.1167/tvst.9.6.8