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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.

To investigate which cytokines, chemokines and growth factors are involved in the immunopathogenesis of idiopathic uveitis, and whether cytokine profiles are associated with. Serum and aqueous humor (AH) samples of 75 patients with idiopathic uveitis were analyzed by multiplex immunoassay. Infectious controls consisted of 16 patients with ocular toxoplasmosis all confirmed by intraocular fluid analyses. Noninfectious controls consisted of 7 patients with Behçet disease related uveitis and 15 patients with sarcoidosis related uveitis. The control group consisted of AH and serum samples from 47 noninflammatory control patients with age-related cataract. In each sample, 27 immune mediators ± IL-21 and IL-23 were measured. In idiopathic uveitis, 13 of the 29 mediators, including most proinflammatory and vascular mediators such as IL-6, IL-8, IL-12, G-CSF, GM-CSF, MCP-1, IP-10, TNF-α and VEGF, were significantly elevated in the aqueous humor when compared to all controls. Moreover, IL-17, IP-10, and IL-21, were significantly elevated in the serum when compared to all controls. We clustered 4 subgroups of idiopathic uveitis using a statistical analysis of hierarchical unsupervised classification, characterized by the order of magnitude of concentrations of intraocular cytokines. The pathogenesis of idiopathic uveitis is characterized by the presence of predominantly proinflammatory cytokines and chemokines and vascular endothelial growth factor with high expression levels as compared to other causes of uveitis. There are indications for obvious Th-1/ IL21-Th17 pathways but also IL9-Th9 and increased IFN-γ-inducing cytokine (IL12) and IFN-γ-inducible CXC chemokine (IP-10). The combined data suggest that immune mediator expression is different among idiopathic uveitis. This study suggests various clusters among the idiopathic uveitis group rather than one specific uveitis entity.