SDG 03 Group - Good Health & Well-being, Landmark University, Omu-Aran, 251101, Kwara State, Nigeria.
Department of Biochemistry, Medicinal Biochemistry, Nanomedicine & Toxicology Laboratory, Landmark University, PMB 1001, Omu-Aran, 251101, Nigeria.
Mol Biol Rep. 2023 Sep;50(9):7851-7865. doi: 10.1007/s11033-023-08688-8. Epub 2023 Jul 30.
Asthma is a prolonged inflammatory disorder of the airways, that affects an estimated 300 million people worldwide. Asthma is triggered by numerous endogenous and exogenous stimuli with symptoms like wheezing, cough, short of breath, chest tightening, airway obstruction, and hyperreactivity observed in patients.
The review seeks to identify targets of redox imbalance and inflammation that could be explored to create effective treatments for asthma.
The methodology involved a search and review of literature relating to asthma pathogenesis, redox homeostasis, and inflammation.
Eosinophils and neutrophils are involved in asthma pathogenesis. These inflammatory cells generate high levels of endogenous oxidants such as hydrogen peroxide and superoxide, which could result in redox imbalance in the airways of asthmatics. Redox imbalance occurs when the antioxidant systems becomes overwhelmed resulting in oxidative stress. Oxidative stress and inflammation have been linked with asthma inflammation and severity. Reactive oxygen species (ROS)/reactive nitrogen species (RNS) cause lung inflammation by activating nuclear factor kappa-B (NF-κB), mitogen-activated protein kinase (MAPK), activator protein-1, as well as additional transcription factors. These factors stimulate cytokine production which ultimately activates inflammatory cells in the bronchi, causing lung cellular injury and destruction. ROS/RNS is also produced by these inflammatory cells to eradicate invading bacteria. Antioxidant treatments for asthma have not yet been fully explored.
Redox and inflammatory processes are viable targets that could be explored to create better therapy for asthma.
哮喘是一种气道的慢性炎症性疾病，全球估计有 3 亿人受其影响。哮喘由许多内源性和外源性刺激物引发，患者会出现喘息、咳嗽、呼吸急促、胸闷、气道阻塞和高反应性等症状。
本综述旨在确定可能成为治疗哮喘有效方法的氧化还原失衡和炎症靶点。
本研究采用搜索和综述与哮喘发病机制、氧化还原平衡和炎症相关的文献的方法。
嗜酸性粒细胞和中性粒细胞参与哮喘发病机制。这些炎症细胞会产生高水平的内源性氧化剂，如过氧化氢和超氧化物，这可能导致哮喘患者气道中的氧化还原失衡。当抗氧化系统不堪重负导致氧化应激时，就会发生氧化还原失衡。氧化应激和炎症与哮喘炎症和严重程度有关。活性氧（ROS）/活性氮（RNS）通过激活核因子 kappa-B（NF-κB）、丝裂原活化蛋白激酶（MAPK）、激活蛋白-1 以及其他转录因子，引起肺部炎症。这些因素刺激细胞因子的产生，最终激活支气管中的炎症细胞，导致肺细胞损伤和破坏。这些炎症细胞也会产生 ROS/RNS 来消灭入侵的细菌。针对哮喘的抗氧化治疗尚未得到充分探索。
氧化还原和炎症过程是可行的靶点，可以探索更好的哮喘治疗方法。
