It is good to see some research that is actually improving lung function. Still has a ways to go but it is definitely a start.
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Protectin DX Found to Reverse Fibrotic Process in Mice with Lung Fibrosis
Results from a preclinical study showed that treatment with a fatty acid molecule called protectin DX (PDX) could resolve several key features of lung fibrosis in mice.
The results were published in a study titled “Posttreatment with Protectin DX ameliorates bleomycin-induced pulmonary fibrosis and lung dysfunction in mice” in the journal Scientific Reports. This report demonstrates the therapeutic potential of PDX against fibrotic processes.
PDX is a fat molecule that belongs to a class of fatty acids known as specialized pro-resolving mediators. This class of molecules has very important signaling properties with a major role in inflammation resolution.
With potent anti-inflammatory activity and the capacity to modulate immune system cells response, specialized pro-resolving mediators such as PDX are attractive therapeutic tools for the treatment of inflammatory medical conditions.
In the current study, the authors evaluated the beneficial effects of PDX on mouse models of lung fibrosis.
Treatment with PDX after lung fibrosis in mice was shown to efficiently reduce infiltration of inflammatory cells, destruction of lung structure, and deposition of collagen fibers, all key features of fibrosis.
In addition, activity in the lungs of pro-inflammatory proteins such as IL- 1β, IL-17, TNF-α, and TGF-β was found to be significantly reduced upon PDX treatment, compared to levels found in untreated mice.
Besides these beneficial effects at the molecular level of the fibrotic process, treatment with PDX also showed potential therapeutic benefits in long-term outcome effects. Treatment not only improved the respiratory capacity and overall blood oxygenation of mice, it also prolonged their live span.
Overall, these findings showed that post-treatment with PDX could improve and reverse pulmonary fibrosis as well as lung function in mice, suggesting that PDX might be a potential therapeutic tool for fibrotic lung diseases.
“These data have significant implications for future efforts in developing an efficient therapeutic strategy for treating lung fibrosis by targeting PDX actions,” researchers wrote.
Post-treatment strategy is essential to patients with fibrosis, they said.
More studies are needed to fully understand the underlying mechanism of action of PDX and its therapeutic effects in lung fibrosis
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