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Abstract
An imbalance in the production of reactive oxygen species in the body can cause an increase of oxidative stress that leads to oxidative damage to cells and tissues, which culminates in the development or aggravation of some chronic diseases, such as inflammation, diabetes mellitus, cancer, cardiovascular disease, and obesity. Secondary metabolites from Inula species can play an important role in the prevention and treatment of the oxidative stress-related diseases mentioned above. The databases Scopus, PubMed, and Web of Science and the combining terms Inula, antioxidant and secondary metabolites were used in the research for this review. More than 120 articles are reviewed, highlighting the most active compounds with special emphasis on the elucidation of their antioxidative-stress mechanism of action, which increases the knowledge about their potential in the fight against inflammation, cancer, neurodegeneration, and diabetes. Alantolactone is the most polyvalent compound, reporting interesting EC50 values for several bioactivities, while 1-O-acetylbritannilactone can be pointed out as a promising lead compound for the development of analogues with interesting properties. The Inula genus is a good bet as source of structurally diverse compounds with antioxidant activity that can act via different mechanisms to fight several oxidative stress-related human diseases, being useful for development of new drugs.
Highlights
Oxygen metabolism, which involves mainly redox reactions, is fundamental for human life, but it leads to the production of reactive oxygen species (ROS) and reactive nitrogen species (RNS) [1,2], affecting regulation of several biological processes and cell functions [3]
When cellular production of ROS and RNS overwhelms the antioxidant capacity of cells, it leads to a state of oxidative stress, which in turn can cause oxidative damage to large biomolecules such as proteins, lipids, and deoxyribonucleic acid (DNA) [6]
± 0.36 μM, being better than the positive control aminoguanidine (IC50 = 9.12 ± 0.35 μM). These results are in accordance with the ones presented by Chun et al [57], where compound 11 at 10 μM inhibited the production of NO, prostaglandin E2 (PGE2), and tumor necrosis factor-α (TNF-α), as well as Cyclooxygenase 2 (COX-2) and inducible nitric oxide synthase (iNOS) protein and mRNA transcription in LPS-stimulated RAW 264.7 cells
Summary
Oxygen metabolism, which involves mainly redox reactions, is fundamental for human life, but it leads to the production of reactive oxygen species (ROS) and reactive nitrogen species (RNS) [1,2], affecting regulation of several biological processes and cell functions [3]. The antioxidant activity assays by the DPPH and ABTS methods are simple, rapid, and very useful as a first approach, the extrapolation of their results to the antioxidant effect at a cellular level in a biological environment is impossible, and they do not give any information about the cellular mechanisms in which the compounds tested act. This information is very relevant and is obtained using methods and approaches very different from those discussed so far. We present not an exhaustive compilation but rather a critical analysis of the more in-depth studies and the most relevant aspects of the action mechanisms exhibited by the Inula compounds that have, as a final consequence, the reduction of the oxidative stress nature inherent to the mentioned diseases
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