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Study on the relationship between apigenin and human health

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Study on the relationship between apigenin and human health

2025-01-21

Research results sharing

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01 Natural flavonoid apigenin, an effective drug against nervous system cancer

Abstract:

Cancer is a serious public health problem worldwide, and nervous system (NS) cancer is one of the most life-threatening malignancies. Efforts have been made to introduce natural anticancer agents with minimal side effects. Apigenin is an edible flavonoid that is abundant in many vegetables and fruits. Apigenin has a variety of pharmacological activities, including antioxidant, antimicrobial and anticancer effects. This article reviews the therapeutic effects of apigenin and structurally similar flavonoids on glioblastoma and neuroblastoma. Current evidence shows that apigenin has a unique ability to cross the blood-brain barrier, and its antioxidant, anti-aging, neurogenic and neuroprotective effects make this flavonoid an excellent choice for the treatment of neurodegenerative diseases. Apigenin has low toxicity to normal nerve cells, but its killing effect on NS cancer cells is achieved by activating multiple signaling pathways and molecular targets. The anti-tumor mechanism of apigenin includes inducing cell cycle arrest and apoptosis, inhibiting cell migration, invasion and angiogenesis, etc. Apigenin is a promising drug, but its low bioavailability is an important issue that must be addressed before its clinical application. Recently, nanodelivery of apigenin by liposomes and poly(lactic-co-glycolide) nanoparticles has greatly improved the functionality of this agent. Therefore, studying the drug effects of apigenin-loaded nanocarriers on NS cancer cell lines and animal models is a suggestion for future research.

Conclusion:

As a naturally occurring flavonoid, apigenin has shown anticancer efficacy against a variety of human malignancies, including NS cancer. The low toxicity of apigenin to neuronal cells, along with the broad range of signaling pathways and targets that it simultaneously triggers in glioblastoma and neuroblastoma cells, demonstrates the role of apigenin as a promising agent. However, the low bioavailability of apigenin is an important issue that must be addressed before introducing this valuable flavonoid into the clinic. So far, the anticancer activity of apigenin has been mainly studied in vitro and in animal models, while clinical studies on other beneficial effects of apigenin, such as its neuroprotective effects, are very limited. The main reason limiting the clinical trials of apigenin is its very low solubility in water and non-polar solvents, as well as its high permeability and degradability. To overcome the poor bioavailability of apigenin and improve its functionality, the use of nanocarriers is an interesting strategy. It is therefore recommended to investigate the drug effects of nanocarriers loaded with apigenin on NS cancer cell lines and animal models in future studies.

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02 Apigenin targets fetuin-A to improve obesity-induced insulin resistance

Abstract:

Fetuin-A is a hepatocyte factor secreted by hepatocytes that binds to insulin receptors, thereby impairing the activation of the insulin signaling pathway, leading to insulin resistance. Apigenin is a flavonoid isolated from plants that has beneficial effects on insulin resistance; however, its regulatory mechanisms are not fully understood. In this study, the molecular mechanisms of the protective effect of apigenin on insulin resistance were investigated. In Huh7 cells, apigenin treatment decreased fetuin-A mRNA expression by reducing ROS-mediated casein kinase 2α (CK2α)-nuclear factor kappa light chain activated enhancer B activation; moreover, apigenin reduced CK2α-dependent fetuin-A phosphorylation levels, thereby promoting fetuin-A degradation through the autophagic pathway, leading to decreased fetuin-A protein levels. In addition, apigenin prevented the formation of fetuin-A-insulin receptor (IR) complexes, thereby rescuing the palmitate (PA)-induced impaired insulin signaling pathway, as evidenced by increased phosphorylation of IR substrate-1 and Akt, and glucose transporter 2 from the cytosol to the plasma membrane. Similar results were observed in the livers of HFD-fed mice treated with apigenin. Collectively, the findings suggest that apigenin improves obesity-induced hepatic insulin resistance by targeting fetuin-A.

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Conclusion:

The results indicate that hepatocytes exposed to excessive PA rapidly increase ROS production and induce activation of the CK2α-NF-κB pathway, which in turn upregulates fetuin-A mRNA expression. In addition, PA-activated CK2α led to an increase in the phosphorylated form of fetuin-A protein, thereby prolonging its half-life. Transcriptional and post-translational regulation may jointly upregulate the level of fetuin-A in hepatocytes. In addition, apigenin abolished the PA-induced increase in fetuin-A protein levels by inhibiting the generation of ROS and CK2α-dependent transcriptional and post-translational regulation. Therefore, apigenin prevented the PA-induced increase in fetuin-A expression and the formation of fetuin-A-IR complex, thereby rescuing the PA-induced impairment of hepatocyte insulin signaling and glucose uptake. Apigenin reduced the phosphorylated serine level of fetuin-A induced by PA or HFD. By regulating the function of fetuin-A, through transcriptional and post-translational pathways. The molecular mechanism by which apigenin regulates CK2α and NF-κB activation in hepatocytes needs further study. In conclusion, this study demonstrates a unique protective mechanism of apigenin in the treatment of hepatic insulin resistance, involving the regulation of fetuin A gene expression and fetuin A protein phosphorylation, as well as the interaction between fetuin A and IR, ultimately leading to the alleviation of obesity-induced hepatocyte and hepatic insulin resistance.

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03 Effect of apigenin on gastric cancer cells

Abstract:

Gastric cancer (GC) is one of the most common cancers worldwide. As currently available treatment options are invasive, new and more benign options are being explored. One of these 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, antioxidant, and antiproliferative properties in several diseases, and its potential as an anticancer compound has been explored. Here, this paper systematically organizes the existing data on the effects of Api on GC cells, including cell proliferation, apoptosis, Helicobacter pylori infection, and molecular targets. From the literature, it can be concluded that Api inhibits cell growth in a dose- and time-dependent manner, which is accompanied by a reduction in clonogenicity and the induction of apoptosis. This occurs via the Akt/Bad/Bcl2/Bax axis, which activates the mitochondrial pathway of apoptosis, leading to the limitation of cell proliferation. Moreover, it seems that the antiproliferative potential of Api on GC cells is particularly relevant to the more aggressive GC phenotype, but can also affect normal gastric cells. This suggests that this flavonoid must be used in low to moderate doses to avoid side effects caused by the interference of the normal epithelium. In H. pylori infected cells, the literature suggests that Api reduces inflammation by reducing the level of H. pylori colonization, preventing NF-kB activation and reducing the production of reactive oxygen species (ROS). Therefore, in GC Api seems to modulate different cancer hallmarks such as cell proliferation, apoptosis, cell migration, inflammation and oxidative stress, demonstrating its potential as an anti-GC compound.

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Conclusion:

For centuries, natural products have been used worldwide as therapeutic agents to treat inflammatory diseases. Currently, in vitro and in vivo experiments with flavonoids or other plant-derived components are being conducted to reveal further health benefits of these phytochemicals. Accumulating evidence suggests that Api is a natural flavonoid with a wide range of pharmacological activities and has great therapeutic value against different types of cancer. In GC, when present at low to moderate doses, Api appears to have the ability to reduce colony formation and inhibit cell proliferation in a dose- and time-dependent manner, with more pronounced effects in undifferentiated cells, without altering normal gastric epithelium. Moreover, the growth inhibitory activity of Api in GC cells is at least partially associated with the induction of apoptosis. In in vivo studies, Api can reduce inflammation in vitro, atrophic gastritis and gastric cancer, and colonization of gastric epithelium by H. pylori in H. pylori-infected gastric epithelium. Moreover, API appears to be a multi-targeted drug, as it can modulate key factors and important signaling pathways, such as Akt/Bad/Bax and IkBα/NF-kB, which are involved in tumor initiation and progression, as demonstrated by in vitro and in vivo studies; as well as the levels of ROS in GC cells. In conclusion, according to the studies included in this review, in the context of GC, API has the ability to modulate different hallmarks of cancer, such as cell proliferation, apoptosis, inflammation, and oxidative stress.

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04 Apigenin: A natural molecule at the intersection of sleep and aging

Abstract:

NAD+ is a key coenzyme of metabolism that exhibits a characteristic decline with age. In mice, NAD+ levels can be elevated by treatment with apigenin, a natural flavonoid that inhibits the NAD+-consuming glycoprotein CD38. In animal models, apigenin has positive effects on both sleep and lifespan. For example, apigenin improves learning and memory in aged mice, reduces tumor proliferation in a mouse xenograft model of triple-negative breast cancer, and induces sedation in mice and rats. In addition, apigenin prolongs survival in a fly model of neurodegenerative diseases, and apigenin glycosides increase lifespan in worms. The therapeutic potential of apigenin is emphasized by human clinical studies using chamomile extracts, which contain apigenin as the active ingredient. Overall, chamomile extracts have been reported to relieve anxiety, improve mood, and relieve pain. In addition, dietary apigenin intake is positively correlated with sleep quality in adults. The electron-rich flavonoid structure of apigenin gives it the ability to form strong bonds with different molecular structures of receptors and enzymes. The effects of apigenin extend beyond CD38 inhibition to include both agonistic and antagonistic modulation of various targets, including GABA and inflammatory pathways. A wealth of evidence positions apigenin as a unique molecule capable of influencing aging and sleep. Further research is necessary to better understand the nuanced mechanisms and clinical potential of apigenin.

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Conclusion:

Despite numerous studies confirming the longevity-promoting and sleep-promoting properties of apigenin, a number of important questions remain. First, given the promiscuous nature of the binding of flavonoid polyphenols and the broad systemic effects of apigenin, additional work is needed to determine, for example, whether additional targets for apigenin exist; the optimal dose and safety profile over longer treatment periods and in different patient populations; the biological effects of all known chemical derivatives of apigenin and the extent to which each contributes to the health benefits described herein. In addition, because apigenin is poorly absorbed in the small intestine, the therapeutic effects of apigenin could potentially be enhanced by improving its bioavailability. However, the potential benefits of increased absorption of apigenin in the small intestine must be weighed against the reduced availability of apigenin for microbial conversion to smaller phenolic metabolites in the large intestine, which, as mentioned earlier, are also absorbed into the circulation and may have effects on sleep and aging. In addition, not all mechanisms for increasing NAD+ levels are equally beneficial or effective. For example, increasing NAD+ levels by inhibiting CD38, an immune cell glycoprotein, may be preferable to increasing NAD+ levels by inhibiting PARP1, an enzyme that responds to DNA damage and promotes DNA repair. A systematic comparison and risk/benefit analysis of different interventions to increase NAD+ levels would be valuable. Finally, further research is needed to elucidate the mechanism of action of apigenin.

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