Meng Ting, Li Feng-Sen, Xu Dan, Jing Jing, Li Zheng, Maimaitiaili Miyesier, Bao Yong-Jiang
College of Traditional Chinese Medicine, Xinjiang Medical University, Urumqi, China.
Department of General Medicine, The Eighth People's Hospital of Xinjiang Uygur Autonomous Region, Urumqi, China.
J Thorac Dis. 2024 Apr 30;16(4):2326-2340. doi: 10.21037/jtd-23-1115. Epub 2024 Apr 16.
Chronic obstructive pulmonary disease (COPD) is a heterogeneous group of pathophysiological bases of airway inflammation and its anti-inflammatory response. Aberrant mitochondrial signaling and mitochondrial dysfunction underlie the pathomechanisms leading to COPD. This study aims to investigate the effects of the Yiqigubiao (YQGB) pill, a traditional Chinese medicine (TCM), on Sirtuin 5 (SIRT5) and mitochondrial function in patients with COPD.
Thirty-four patients with COPD were randomized into oral YQGB or placebo groups concurrent with a 24-week routine treatment. The pulmonary function was assessed by examining the levels of forced expiratory volume in one second (FEV)/forced vital capacity (FVC), FEV, and FVC. Quantitative real-time polymerase chain reaction (qRT-PCR) and Western blot were used to detect SIRT5 expression in mitochondria isolated from peripheral blood. Flow cytometry was used to detect changes in mitochondrial membrane potential and reactive oxygen species (ROS) in peripheral blood lymphocytes. Human bronchial epithelial (HBE) cells stimulated by cigarette smoke extract (CSE) were treated with YQGB. After SIRT5 was knocked down in cells, the changes in mitochondrial membrane potential, levels of adenosine triphosphate (ATP), and ROS were detected.
YQGB treatment significantly improved lung function in patients with COPD. The expression of SIRT5 and the mitochondrial membrane potential significantly increased and ROS decreased in patients with COPD after YQGB treatment. The CSE decreased cell proliferation and SIRT5 expression, which was alleviated after YQGB treatment. Furthermore, SIRT5 was knocked down in CSE-stimulated HBE cells, and its expression was elevated upon YQGB treatment. The knockdown of SIRT5 significantly altered the CSE-stimulation-induced dysregulation of mitochondrial membrane potential, ATP levels, and ROS. This was also restored after YQGB treatment.
YQGB treatment can elevate SIRT5 expression, restore mitochondrial function in COPD, and exert protective effects.
慢性阻塞性肺疾病（COPD）是一组具有气道炎症及其抗炎反应病理生理基础的异质性疾病。异常的线粒体信号传导和线粒体功能障碍是导致COPD的发病机制基础。本研究旨在探讨中药益气固表（YQGB）丸对COPD患者沉默调节蛋白5（SIRT5）和线粒体功能的影响。
34例COPD患者被随机分为口服YQGB组或安慰剂组，同时进行为期24周的常规治疗。通过检测一秒用力呼气容积（FEV）/用力肺活量（FVC）、FEV和FVC水平来评估肺功能。采用定量实时聚合酶链反应（qRT-PCR）和蛋白质印迹法检测外周血分离线粒体中SIRT5的表达。采用流式细胞术检测外周血淋巴细胞线粒体膜电位和活性氧（ROS）的变化。用香烟烟雾提取物（CSE）刺激人支气管上皮（HBE）细胞后用YQGB处理。在细胞中敲低SIRT5后，检测线粒体膜电位、三磷酸腺苷（ATP）水平和ROS的变化。
YQGB治疗显著改善了COPD患者的肺功能。YQGB治疗后，COPD患者SIRT5的表达及线粒体膜电位显著升高，ROS降低。CSE降低了细胞增殖和SIRT5表达，YQGB治疗后得到缓解。此外，在CSE刺激的HBE细胞中敲低SIRT5，YQGB处理后其表达升高。敲低SIRT5显著改变了CSE刺激引起的线粒体膜电位、ATP水平和ROS的失调。YQGB治疗后也恢复了这些指标。
YQGB治疗可提高SIRT5表达，恢复COPD患者的线粒体功能，并发挥保护作用。
