Electroacupuncture ameliorates cardiopulmonary bypass induced apoptosis in lung via ROS/Nrf2/NLRP3 inflammasome pathway

• Published in: Life sciences (1973) 2019-12, Vol.238, p.116962-116962, Article 116962
• Main Authors: Dhar, Rana, Zhang, Lejun, Li, Yajun, Rana, Mohammad Nasiruddin, Hu, Zhengqiang, Li, Zigang, Cui, Huashun, Tang, Huifang
• Format: Article
• Language: English
• Subjects: Activation; Acupuncture; Acute Lung Injury - etiology; Acute Lung Injury - metabolism; Acute Lung Injury - pathology; Acute Lung Injury - prevention & control; Animals; Apoptosis; Cardiopulmonary bypass; Cardiopulmonary Bypass - adverse effects; Caspase-8; Cytokines; Electroacupuncture - methods; Heart surgery; IL-1β; Inflammasome; Inflammasomes; Inflammation; Interleukins; Lungs; Macrophages; Male; Molecular modelling; NF-E2-Related Factor 2 - metabolism; NLR Family, Pyrin Domain-Containing 3 Protein - metabolism; Nrf2; Proteins; Rats; Rats, Sprague-Dawley; Reactive Oxygen Species - metabolism; ROS; Tumor necrosis factor-TNF; Tumor necrosis factor-α
• ISSN: 0024-3205; 1879-0631
• DOI: 10.1016/j.lfs.2019.116962

Electroacupuncture (EAc) has a pulmonary protective effect during cardiopulmonary bypass (CPB), but its molecular mechanisms including inflammasome activation signaling pathways remains unclear. Male Sprague Dawley rats were divided into control, CPB + EAc and CPB groups. Lung injury model was developed by CPB treatment and EAc (2/100 Hz) was carried out before CPB in the CPB + EAc group. Lung tissues were collected at two time points (0.5 h; 2 h) to determine cytokines release by ELISA kits, and protein expressions by Western blot. Serum collected at two time points (0.5 h; 2 h) from CPB and CPB + EAc treated groups were used in NR8383 cells to confirm the effect of EAc. CPB significantly increased the inflammatory mediators, histological damage and expression of inflammasome related protein and apoptosis, when compared with control group. The level of tumor necrosis factor-α(TNF-α), interleukin (IL)-18 and IL-1β in the CPB + EAc treated group was significantly decreased along with histological changes compared to CPB. Moreover, EAc inhibited the activation of Nod like receptor protein-3 (NLRP3) inflammasome complex, caspase-8 and activated NF-E2-related factor 2 (p-Nrf2). In addition, serum from the CPB + EAc group prevented CPB induced activation of inflammasome and related mediators, reducing ROS generation and apoptosis in NR8383 macrophages. These findings indicate that EAc had a critical anti-apoptotic role by suppression of ROS/Nrf2/NLRP3 inflammasome pathway. EAc might be a possible therapeutic treatment for CPB-induced acute lung injury. [Display omitted]