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Biomedicine & Pharmacotherapy =... Aug 2023Prolonged exposure to UV light can lead to photo-ageing of the skin. Therefore, the development and application of anti-photoaging drugs is urgent. In this study, we...
Prolonged exposure to UV light can lead to photo-ageing of the skin. Therefore, the development and application of anti-photoaging drugs is urgent. In this study, we co-loaded apigenin (Apn) and doxycycline (Doc), a broad-spectrum inhibitor of matrix metalloproteinases (MMPs), into flexible liposomes to exert anti-photoaging effects by combating oxidative stress, anti-inflammation, reducing the activation of MMPs and preventing collagen loss. The results showed that we prepared a flexible liposome (A/D-FLip) containing Apn and Doc. Its appearance, particle size and Zeta potential were normal and it had good encapsulation efficiency, drug loading, in vitro release and transdermal efficiency. In cellular experiments, A/D-FLip could inhibit oxidative stress damage, reduce inflammatory factors and decrease the activation of MMPs in Human immortalized keratinocytes (HaCaT) cells; in animal experiments, A/D-FLip could inhibit skin damage and reduce skin collagen loss by decreasing the activation of MMPs, thus inhibiting skin photoaging in mice. In conclusion, A/D-FLip has good anti-photoaging effects and it has the potential to become an effective skin care product or drug against UV damage and skin photoaging in the future.
Topics: Animals; Mice; Humans; Liposomes; Apigenin; Doxycycline; Skin; Collagen; Skin Aging; Matrix Metalloproteinases; Ultraviolet Rays
PubMed: 37301137
DOI: 10.1016/j.biopha.2023.114998 -
Biomedicine & Pharmacotherapy =... Mar 2024Gastric Cancer (GC) is one of the most prevalent cancers worldwide. As the currently available therapeutic options are invasive, new and more benign options are being... (Review)
Review
Gastric Cancer (GC) is one of the most prevalent cancers worldwide. As the currently available therapeutic options are invasive, new and more benign options are being explored. One of which is Apigenin (Api), a natural flavonoid found in fruits and vegetables, such as celery, parsley, garlic, bell pepper and chamomile tea. Api has known anti-inflammatory, -oxidant, and -proliferative proprieties in several diseases and its potential as an anticancer compound has been explored. Here we systematize the available data regarding the effects of Api on GC cells, in terms of cell proliferation, apoptosis, Helicobacter pylori (H. pylori) infection, and molecular targets. From the literature it is possible to conclude that Api inhibits cell growth in a dose- and time-dependent manner, which is accompanied by the reduction of clone formation and induction of apoptosis. This occurs through the Akt/Bad/Bcl2/Bax axis that activates the mitochondrial pathway of apoptosis, resulting in restriction of cell proliferation. Additionally, it seems that the anti-proliferative potential of Api on GC cells is particularly relevant in a more aggressive GC phenotype but can also affect normal gastric cells. This indicate that this flavonoid must be used in low-to-moderate doses to avoid side-effects induced by disturbance of the normal epithelium. In H. Pylori-infected cells, the literature demonstrates that Api reduces inflammation by diminishing the levels of H. pylori colonization, by preventing NF-kB activation and by diminishing the production of reactive oxygen specimens (ROS). Accordingly, in GC Api seems to regulate different hallmarks of cancer, such as cell proliferation, apoptosis, cell migration, inflammation and oxidative stress, demonstrating its potential has an anti-GC compound.
Topics: Humans; Stomach Neoplasms; Apigenin; Apoptosis; Antioxidants; Inflammation
PubMed: 38330709
DOI: 10.1016/j.biopha.2024.116251 -
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 -
Nutrients Aug 2020This review summarizes the latest advancements in phytochemicals as functional antiviral agents. We focused on flavonoids, like apigenin, vitexin, quercetin, rutin and... (Review)
Review
This review summarizes the latest advancements in phytochemicals as functional antiviral agents. We focused on flavonoids, like apigenin, vitexin, quercetin, rutin and naringenin, which have shown a wide range of biological effects including antiviral activities. The molecular mechanisms of their antiviral effects mainly consist in the inhibition of viral neuraminidase, proteases and DNA/RNA polymerases, as well as in the modification of various viral proteins. Mixtures of different flavonoids or combination of flavonoids with antiviral synthetic drugs provide an enhancement of their antiviral effects. Recent strategies in drug delivery significantly contribute to overcoming the low bioavailability of flavonoids. Frequent viral infections worldwide have led to the need for new effective antiviral agents, which can be identified among the various phytochemicals. In this light, screening the antiviral activities of a cocktail of flavonoids would be advantageous in order to prevent viral infections and improve current antiviral therapies.
Topics: Antiviral Agents; Apigenin; Biological Availability; Drug Combinations; Drug Delivery Systems; Drug Evaluation, Preclinical; Drug Synergism; Flavanones; Flavonoids; Humans; Neuraminidase; Quercetin; Rutin; Viral Protease Inhibitors; Viral Proteins; Virus Diseases; Viruses
PubMed: 32825564
DOI: 10.3390/nu12092534 -
Frontiers in Cellular and Infection... 2023Current treatment for visceral leishmaniasis is based on drugs such as pentavalent antimony and amphotericin B. However, this treatment remains mostly ineffective and...
Current treatment for visceral leishmaniasis is based on drugs such as pentavalent antimony and amphotericin B. However, this treatment remains mostly ineffective and expensive, resulting in several side effects and generating resistance. Apigenin, a flavonoid present in fruits and vegetables, has demonstrated several biological functions. In the present study, we observed a concentration-dependent inhibition of the promastigote in the presence of apigenin, exhibiting an IC value of 29.9 µM. Its effect was also evaluated in -infected murine peritoneal macrophages, presenting an C value against intracellular amastigotes of 2.3 µM and a selectivity index of 34.3. In a murine model of visceral leishmaniasis, the effect of apigenin was measured using short-term and long-term treatment schemes. Treatment with apigenin demonstrated 99.7% and 94% reductions in the liver parasite load in the short-term and long-term treatment schemes, respectively. Furthermore, no alterations in serological and hematological parameters were observed. Taken together, these results suggest that apigenin is a potential candidate for visceral leishmaniasis chemotherapy by oral administration.
Topics: Animals; Mice; Leishmaniasis, Visceral; Apigenin; Leishmania infantum; Amphotericin B; Antiprotozoal Agents; Mice, Inbred BALB C
PubMed: 37091674
DOI: 10.3389/fcimb.2023.1066407 -
Journal of Integrative Neuroscience May 2023Apigenin has been reported to exhibit anti-inflammatory and anti-oxidative activities. This study aimed to investigate the protective role of Apigenin on...
BACKGROUND
Apigenin has been reported to exhibit anti-inflammatory and anti-oxidative activities. This study aimed to investigate the protective role of Apigenin on chemotherapy-induced peripheral neuropathy (CIPN).
METHODS
CIPN mouse model was established using Paclitaxel treatment. Hot plate and tail prick latency tests were performed to examine the allodynia and hyperalgesia behaviors. Anti-inflammatory and anti-oxidative effects of Apigenin on CIPN were determined by enzyme-linked immunosorbent (ELISA) assay, Western blot, and qRT-PCR. Nuclear recruitment of nuclear factor erythroid 2-related factor 2 (NRF2) was analyzed to evaluate the underlying mechanisms of the protective effects of Apigenin.
RESULTS
Apigenin significantly alleviated CIPN-induced nociceptive behaviors of CIPN mice. It also decreased the TNF-α and IL-1β levels, suppressed oxidative stress and inflammation in the surgical spinal cord tissues. Mechanistically, Apigenin altered the pro-inflammatory and anti-inflammatory phenotypes ratio of microglia through promoting the nuclear recruitment of NRF2 and activating the NRF2/Antioxidant Response Element (ARE) signaling pathway.
CONCLUSIONS
In summary, Apigenin relieves CIPN by regulating microglia activation and polarization, which provides a potential therapeutic strategy for CIPN treatment.
Topics: Mice; Animals; Hyperalgesia; Apigenin; Microglia; NF-E2-Related Factor 2; Peripheral Nervous System Diseases; Anti-Inflammatory Agents; Antineoplastic Agents
PubMed: 37258427
DOI: 10.31083/j.jin2203064 -
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 -
International Journal of Molecular... May 2024Due to its propensity to metastasize, cancer remains one of the leading causes of death worldwide. Thanks in part to their intrinsic low cytotoxicity, the effects of the... (Review)
Review
Due to its propensity to metastasize, cancer remains one of the leading causes of death worldwide. Thanks in part to their intrinsic low cytotoxicity, the effects of the flavonoid family in the prevention and treatment of various human cancers, both in vitro and in vivo, have received increasing attention in recent years. It is well documented that Apigenin (4',5,7-trihydroxyflavone), among other flavonoids, is able to modulate key signaling molecules involved in the initiation of cancer cell proliferation, invasion, and metastasis, including JAK/STAT, PI3K/Akt/mTOR, MAPK/ERK, NF-κB, and Wnt/β-catenin pathways, as well as the oncogenic non-coding RNA network. Based on these premises, the aim of this review is to emphasize some of the key events through which Apigenin suppresses cancer proliferation, focusing specifically on its ability to target key molecular pathways involved in angiogenesis, epithelial-to-mesenchymal transition (EMT), maintenance of cancer stem cells (CSCs), cell cycle arrest, and cancer cell death.
Topics: Apigenin; Humans; Neoplasms; Animals; Epithelial-Mesenchymal Transition; Signal Transduction; Cell Proliferation; Neoplastic Stem Cells; Neovascularization, Pathologic
PubMed: 38791608
DOI: 10.3390/ijms25105569 -
International Journal of Molecular... Feb 2023The prominent flavonoids apigenin and chrysin have been demonstrated to have systemic benefits. Our previous work was first to establish the impact of apigenin and...
The prominent flavonoids apigenin and chrysin have been demonstrated to have systemic benefits. Our previous work was first to establish the impact of apigenin and chrysin on cellular transcriptome. In the current study, we have revealed the ability of apigenin and chrysin to alter the cellular metabolome based on our untargeted metabolomics. Based on our metabolomics data, both these structurally related flavonoids demonstrate diverging and converging properties. Apigenin demonstrated the potential to possess anti-inflammatory and vasorelaxant properties through the upregulation of intermediate metabolites of alpha-linolenic acid and linoleic acid pathways. Chrysin, on the other hand, exhibited abilities to inhibit protein and pyrimidine synthesis along with downregulation of gluconeogenesis pathways based on the altered metabolites detected. Chrysin-mediated metabolite changes are mostly due to its ability to modulate L-alanine metabolism and the urea cycle. On the other hand, both the flavonoids also demonstrated converging properties. Apigenin and chrysin were able to downregulate metabolites involved in cholesterol biosynthesis and uric acid synthesis, namely 7-dehydrocholesterol and xanthosine, respectively. This work will provide understanding regarding the diverse therapeutic potential of these naturally occurring flavonoids and help us in curbing an array of metabolic complications.
Topics: Apigenin; Flavonoids; Up-Regulation; Metabolomics
PubMed: 36835484
DOI: 10.3390/ijms24044066 -
Proceedings of the National Academy of... Nov 2021Vascular endothelial cells are exposed to shear stresses with disturbed vs. laminar flow patterns, which lead to proinflammatory vs. antiinflammatory phenotypes,...
Vascular endothelial cells are exposed to shear stresses with disturbed vs. laminar flow patterns, which lead to proinflammatory vs. antiinflammatory phenotypes, respectively. Effective treatment against endothelial inflammation and the consequent atherogenesis requires the identification of new therapeutic molecules and the development of drugs targeting these molecules. Using Connectivity Map, we have identified vitexin, a natural flavonoid, as a compound that evokes the gene-expression changes caused by pulsatile shear, which mimics laminar flow with a clear direction, vs. oscillatory shear (OS), which mimics disturbed flow without a clear direction. Treatment with vitexin suppressed the endothelial inflammation induced by OS or tumor necrosis factor-α. Administration of vitexin to mice subjected to carotid partial ligation blocked the disturbed flow-induced endothelial inflammation and neointimal formation. In hyperlipidemic mice, treatment with vitexin ameliorated atherosclerosis. Using SuperPred, we predicted that apurinic/apyrimidinic endonuclease1 (APEX1) may directly interact with vitexin, and we experimentally verified their physical interactions. OS induced APEX1 nuclear translocation, which was inhibited by vitexin. OS promoted the binding of acetyltransferase p300 to APEX1, leading to its acetylation and nuclear translocation. Functionally, knocking down APEX1 with siRNA reversed the OS-induced proinflammatory phenotype, suggesting that APEX1 promotes inflammation by orchestrating the NF-κB pathway. Animal experiments with the partial ligation model indicated that overexpression of APEX1 negated the action of vitexin against endothelial inflammation, and that endothelial-specific deletion of APEX1 ameliorated atherogenesis. We thus propose targeting APEX1 with vitexin as a potential therapeutic strategy to alleviate atherosclerosis.
Topics: Active Transport, Cell Nucleus; Animals; Apigenin; Atherosclerosis; DNA-(Apurinic or Apyrimidinic Site) Lyase; Endothelial Cells; Human Umbilical Vein Endothelial Cells; Humans; Inflammation; Mice; Phenotype; Phosphorylation; Protein Binding; Signal Transduction; Tumor Necrosis Factor-alpha; p300-CBP Transcription Factors
PubMed: 34810252
DOI: 10.1073/pnas.2115158118