Electroacupuncture ameliorates cardiopulmonary bypass induced apoptosis in lung via ROS/Nrf2/NLRP3 inflammasome pathway
| Autor: | Lejun Zhang, Rana Dhar, Zigang Li, Yajun Li, Mohammad Nasiruddin Rana, Huifang Tang, Zhengqiang Hu, Huashun Cui |
|---|---|
| Rok vydání: | 2019 |
| Předmět: |
Male
0301 basic medicine Inflammasomes NF-E2-Related Factor 2 Acute Lung Injury Apoptosis Pharmacology Lung injury 030226 pharmacology & pharmacy General Biochemistry Genetics and Molecular Biology law.invention Rats Sprague-Dawley 03 medical and health sciences 0302 clinical medicine Western blot law NLR Family Pyrin Domain-Containing 3 Protein Cardiopulmonary bypass Animals Medicine General Pharmacology Toxicology and Pharmaceutics Cardiopulmonary Bypass medicine.diagnostic_test business.industry Interleukin Inflammasome General Medicine Rats Electroacupuncture surgical procedures operative 030104 developmental biology Tumor necrosis factor alpha Reactive Oxygen Species business Inflammasome complex circulatory and respiratory physiology medicine.drug |
| Zdroj: | Life Sciences. 238:116962 |
| ISSN: | 0024-3205 |
| Popis: | 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. |
| Databáze: | OpenAIRE |
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