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Researchers of the University of Seville have proven that a natural compound in extra virgin olive oil reduces inflammation of human cells in the joints. Specifically, they have determined that oleacein reduces this reaction and influences the mechanisms that regulate the activity of certain genes. This finding reinforces its potential as a supportive nutritional strategy to improve quality of life in chronic inflammatory pathologies.
The novelty of the research lies in identifying that oleacein reduces inflammation in cells in vitro, in addition to demonstrating that it acts on the mechanisms that regulate the activity of the genes involved in this biological response. That is, oleacein not only reduces inflammatory signals, but also intervenes in the internal system that ‘decides’ how these processes are activated in the cell.

Inflammation is characteristic in diseases such as psoriatic arthritis or rheumatoid arthritis. The patient’s problem is not only the pain caused by the inflammatory processes, but also that they can end up damaging the joint tissue permanently, over time.
In this work, titled ‘Epigenetic regulation by oleacein mitigates IL-1β-induced inflammation in human SW982 synovial cells’ and published in Food & Functionit was demonstrated, in a test in vitrothat this compound reduces the release of substances that activate and perpetuate this inflammation in joint tissue cells, which reinforces its possible role as complementary support for the treatment of inflammatory joint diseases.
Chronic diseases
To better understand how this process occurs, the team used human synovial cells, which are those that line the inside of the joints and participate directly in the inflammatory process.
The experiment was organized into three groups. A first group of cells was maintained under normal conditions, as a point of comparison. In a second group, the researchers caused artificial inflammation by adding IL-1β, a cytokine – an immune system molecule – that acts as an alarm signal and causes cells to begin producing more inflammatory compounds. In the third group, the cells were pretreated with different concentrations of oleacein and then that same alarm signal was activated. In this way they were able to check if the compound stopped the reaction.
The team used human synovial cellswhich are those that line the inside of the joints and participate directly in the inflammatory process.
When analyzing the results, they observed that ‘activated’ cells, that is, those in which an inflammatory reaction has been caused in the laboratory, produced more markers associated with inflammation and possible deterioration of joint tissue. However, when they treated them with oleacein, that response was much smaller. “That is, the compound managed to significantly reduce several of the biological signals that indicate that inflammation is underway. This means that the reaction of the treated cells was lower,” the researcher from the University of Seville and lead author of the study explains to the Discover Foundation. Rocío Muñoz García.
In addition to measuring the substances that cause inflammation, the team analyzed what happened ‘inside’ the cell when that reaction occurs. “To understand it, we must imagine that our genes are like an instruction book. Not all the pages are always read: some are opened and others remain closed. There are small mechanisms that function as markers or signals and that help decide which instructions are used at each moment. We call this epigenetic changes,” details Rocío Muñoz García.
The study suggests that oleacein influences these control mechanisms. That is, it not only reduces the visible signs of inflammation, but it can also intervene in the system that decides which genes are ‘activated’ when the cell becomes inflamed, as if acting on the internal ‘control panel’ of the inflammatory response.
The authors emphasize that this is a preclinical study and in vitro. Even so, they highlight that these findings help to better understand why compounds in olive oil could be of interest as support in chronic inflammatory diseases such as arthritis and psoriasis. The next step will be to test these effects in models closer to the clinic, more specifically, in cells from real patients.
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