Since inflammation is the result of the immune system's protective response to endogenous signals such as invading pathogens or damaged cells, it has long been implicated in the symptoms of infectious diseases. Inflammation has been reported to be closely associated with the development or exacerbation of several non-communicable diseases. Many chronic diseases, such as cancer, diabetes, cardiovascular disease, autoimmune diseases, and neurodegenerative diseases, arise as a result of tissue damage and genomic changes caused by persistent low-grade inflammation in and around affected tissues or organs. Existing treatments for most of these chronic diseases sometimes have more debilitating effects than the disease itself, necessitating safer, less toxic, and more cost-effective treatment alternatives for patients.
For centuries, flavonoids and their preparations have been used to treat a variety of human diseases, and their continued use has been for a long time. The anti-inflammatory effects of flavonoids on chronic diseases such as cancer, diabetes, cardiovascular diseases and neuritis are particularly concerned about apigenin anti inflammatory, a relatively low toxicity and no mutagenicity of flavonoids, which has significant pharmacodynamics. In addition, central nervous system (CNS) inflammation caused by diseases such as multiple sclerosis (MS) can readily enter circulating lymphocytes, monocytes/macrophages, and dendritic cells (DCs), leading to edema, further inflammation and demyelination. Neuroprotective effects of apigenin anti inflammation and other flavonoids due to the lack of safe anti-inflammatory therapies for CNS-related diseases.
What causes apigenin anti inflammatory? Apigenin dose-dependently inhibits collagenase activity involved in rheumatoid arthritis (RA) and inhibits lipopolysaccharide (LPS)-induced nitric oxide (NO) production in RAW 264.7 macrophages. Apigenin pretreatment also attenuated LPS-induced cyclooxygenase-2 (COX-2) expression. Furthermore, apigenin significantly reduced tumor necrosis factor-a (TNF-a)-induced monocyte adhesion to HUVEC monolayers. Apigenin significantly inhibited TNF-a-stimulated upregulation of vascular cell adhesion molecule 1 (VCAM-1)-, intracellular adhesion molecule-1 (ICAM-1)- and E-selectin-mRNA to basal levels. Taken together, these results suggest the effects of apigenin anti inflammatory, including blocking NO-mediated COX-2 expression and monocyte adhesion. These results further suggest that the effects of apigenin anti inflammatory can be used in the therapeutic management of inflammatory diseases.