O papel do estresse oxidativo na DPOC: conceitos atuais e perspectivas

Abstract

centers such as the city of São Paulo ranges from 6% to over 15%, depending on the diagnostic criteria adopted.(4) The fifth leading cause of death worldwide, COPD will have reached, according to recent estimates, the third position by 2030.(3) The increase in the mortality rate for COPD contrasts with the marked reduction in the mortality rate for diseases such as cancer, IntroductionWorldwide, COPD is a health problem with severe economic and social repercussions; at the personal level, COPD constitutes a major cause of patient disability and of low quality of life for patients and their caregivers.(1,2) According to the World Health Organization, 80 million people suffer from moderate or severe COPD. AbstractWorldwide, COPD is a major cause of morbidity and mortality. The clinical and functional manifestations of COPD result from lung injury occurring through various mechanisms, including oxidative stress, inflammation, protease-antiprotease imbalance and apoptosis. Oxidative stress is central to the pathogenesis of COPD, since it can directly damage lung structures and exacerbate the other mechanisms involved. The cellular and molecular events involved in such lung injury are believed to occur long before the clinical and functional expression of COPD. Although the use of bronchodilators is currently the principal treatment for COPD, bronchodilators have little or no effect on disease progression. A better understanding of the pathogenesis of COPD, together with renewed efforts in basic and clinical research, will allow the diagnosis of COPD at a pre-clinical stage and provide more appropriate monitoring of disease activity, as well as leading to the development of novel therapeutic agents that will effectively prevent the progression of the disease.Keywords: Pulmonary disease, chronic obstructive; Oxidative stress; Oxidants; Antioxidants; Inflammation. ResumoA DPOC é uma causa importante de morbidade e mortalidade em escala global. As manifestações clínicas e funcionais da DPOC resultam de danos pulmonares provocados por um conjunto de mecanismos, incluindo o estresse oxidativo, a inflamação, o desequilíbrio do sistema protease-antiprotease e a apoptose. O estresse oxidativo é central na gênese da DPOC, pois além de provocar dano direto às estruturas pulmonares, amplifica os demais mecanismos. Os eventos celulares e moleculares responsáveis pelo dano pulmonar antecedem em muito a expressão clínica e funcional da DPOC. Os broncodilatadores, principais drogas empregadas atualmente no tratamento da DPOC, não são eficazes em reduzir a progressão da doença. Avanços na compreensão da patogênese da DPOC aliados a esforços renovados na pesquisa básica e clínica deverão permitir sua detecção na fase pré-clínica e possibilitar um monitoramento mais adequado de sua atividade, além de permitir a introdução de novas modalidades de agentes terapêuticos capazes de impedir eficazmente sua progressão.

Effects and Mechanism of Bufei Yishen Formula in a Rat Chronic Obstructive Pulmonary Disease Model

“…Many studies suggested that COPD was related to respiratory, diaphragmatic, and skeletal muscle dysfunction [27, 31–33]. Mitochondrial electron transport-related molecules (NAD/NADH/ADP) are also in relation with redox reactions and oxidative stress, which are known to be the key factors in COPD [33, 34]. In addition, regulation of interleukin expression, involved in inflammation, is also a symptom of COPD [35–37].…”

Nigella sativa Pretreatment in Guinea Pigs Exposed to Cigarette Smoke Modulates In Vitro Tracheal Responsiveness

“…The most important processes causing lung damage are oxidative stress produced by the high concentrations of free radicals in tobacco smoke and cytokine release due to inflammatory response to irritant particles such as tobacco smoke in the airways (21). Smoking and exacerbations of COPD result in decreased antioxidant capacity in plasma that can be explained by the increased radical oxygen species release from peripheral blood neutrophils (22, 23) or decreased levels of major plasma antioxidants such as vitamin C or E in smokers (18, 24).…”

Hyperoxia during one lung ventilation: Inflammatory and oxidative responses

“…Oxidative stress and inflammation were also associated with increased total respiratory resistance in our hyperoxia animals, and studies have shown other clinical complications following oxidative injury as well. 25,33–35 …”