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

  • Life Sci. 2019 Dec 1;238:116962. doi: 10.1016/j.lfs.2019.116962.
Rana Dhar  1 ,  Lejun Zhang  1 ,  Yajun Li  1 ,  Mohammad Nasiruddin Rana  1 ,  Zhengqiang Hu  1 ,  Zigang Li  2 ,  Huashun Cui  3 ,  Huifang Tang  4
Affiliations
  • 1. Department of Pharmacology, School of Basic Medical Sciences, Zhejiang University, Hangzhou, 310058, China.
  • 2. Department of Anesthesiology, Women's Hospital, School of Medicine, Zhejiang University, Hangzhou, 310003, China.
  • 3. Department of Acupuncture, Shuguang Hospital Affiliated to Shanghai University of Traditional Chinese Medicine, Shanghai, China. Electronic address: [email protected].
  • 4. Department of Pharmacology, School of Basic Medical Sciences, Zhejiang University, Hangzhou, 310058, China. Electronic address: [email protected].
PMID: 31628913 DOI: 10.1016/j.lfs.2019.116962
Abstract

Aims: Electroacupuncture (EAc) has a pulmonary protective effect during cardiopulmonary bypass (CPB), but its molecular mechanisms including inflammasome activation signaling pathways remains unclear.

Materials and methods: 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.

Key findings: 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.

Significance: 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.

Keywords
Acupuncture; Apoptosis; Cardiopulmonary bypass; Inflammasome; Nrf2; ROS.
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