RESUMO
Background: The present study investigates the impact of oxidative stress after bariatric surgery in patients with obesity. This field of study has gained great interest in recent years due to the role that oxidative stress plays in metabolic diseases. Obesity, by itself, can generate an increase in reactive oxygen and nitrogen species, intensifying cellular damage and promoting the progression of adverse metabolic conditions. In this context, bariatric surgery emerges as a candidate capable of modifying oxidative stress biomarkers, facilitating the patient's metabolic recovery. Methods: A systematic review was carried out, identifying 30 studies found in databases such as PubMed, Scopus, Web of Science, and Google Scholar. It looked at the link between oxidative stress and recovery after bariatric surgery in patients. The selection of studies was based on the measurement of oxidative stress biomarkers before and after surgical intervention. Results: The results reveal a significant decrease in oxidative stress biomarkers after bariatric surgery. However, a notable variability in antioxidant activity is observed between different patients, as well as a significant influence of comorbidities. Conclusions: Bariatric surgery is postulated as an effective intervention in reducing oxidative stress in patients with obesity, enhancing antioxidant activity and improving patient recovery. This finding highlights the importance of considering oxidative stress management as an integral part of postoperative care, suggesting the need to implement complementary treatment strategies to optimize health outcomes.
RESUMO
Alzheimer's disease is a neurodegenerative pathology whose pathognomonic hallmarks are increased generation of ß-amyloid (Aß) peptide, production of hyperphosphorylated (pTau), and neuroinflammation. The last is an alteration closely related to the progression of AD and although it is present in multiple neurodegenerative diseases, the pathophysiological events that characterize neuroinflammatory processes vary depending on the disease. In this article, we focus on mRNA and non-coding RNA alterations as part of the pathophysiological events characteristic of neuroinflammation in AD and the influence of these alterations on the course of the disease through interaction with multiple RNAs related to the generation of Aß, pTau, and neuroinflammation itself.