Bose Protiti, Bathri Rashmi, Kumar Lalit, Vijayan V K, Maudar K K
Department of Research, Bhopal Memorial Hospital & Research Centre (ICMR), Bhopal, India.
Indian J Med Res. 2015 Sep;142(3):245-60. doi: 10.4103/0971-5916.166529.
Chronic obstructive pulmonary disease (COPD) affect millions of people worldwide and is known to be one of the leading causes of death. The highly sensitive airways protect themselves from irritants by cough and sneeze which propel endogenous and exogenous substances to minimize airway noxious effects. One noxious effect of these substances is activation of peripheral sensory nerve endings of nociceptor neurons innervating these airways lining thus transmitting dangerous signals from the environment to the central nervous system (CNS). Nociceptor neurons include transient receptor potential (TRP) ion channels, especially the vanilloid and ankyrin subfamilies, TRPV1/A1 which can be activated by noxious chemical challenges in models of airways disease. As oxidative stress may activate airways sensory neurons and contribute to COPD exacerbations we sought to review the role that TRP channel activation by oxidative signals may have on airway responses. i0 t would be prudent to target the TRP channels with antagonists and lower systemic oxidative stress with agents that can modulate TRP expression and boost the endogenous levels of antioxidants for treatment and management of COPD.
慢性阻塞性肺疾病(COPD)影响着全球数百万人,是已知的主要死因之一。高度敏感的气道通过咳嗽和打喷嚏来保护自身免受刺激物侵害,咳嗽和打喷嚏会将内源性和外源性物质排出,以尽量减少气道的有害影响。这些物质的一种有害影响是激活支配这些气道内衬的伤害性感受器神经元的外周感觉神经末梢,从而将来自环境的危险信号传递到中枢神经系统(CNS)。伤害性感受器神经元包括瞬时受体电位(TRP)离子通道,特别是香草酸和锚蛋白亚家族,TRPV1/A1在气道疾病模型中可被有害化学刺激激活。由于氧化应激可能激活气道感觉神经元并导致COPD急性加重,我们试图综述氧化信号激活TRP通道可能对气道反应产生的作用。用拮抗剂靶向TRP通道,并使用能够调节TRP表达和提高内源性抗氧化剂水平的药物降低全身氧化应激,对于COPD的治疗和管理可能是谨慎的做法。