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Life Sci. 2019 Dec 1;238:116962. doi: 10.1016/j.lfs.2019.116962. Epub 2019 Oct 16.

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

Author information

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: huashunchoi@126.com.
4
Department of Pharmacology, School of Basic Medical Sciences, Zhejiang University, Hangzhou, 310058, China. Electronic address: tanghuifang@zju.edu.cn.

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

PMID:
31628913
DOI:
10.1016/j.lfs.2019.116962

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