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Protective Effects of Acupuncture in Cardiopulmonary Bypass-Induced Lung Injury in Rats.
Inflammation 2017 August
Acute lung injury caused by cardiopulmonary bypass (CPB) increases the mortality after cardiac surgery. Our previous clinical study suggested that electroacupuncture (EAc) has a protective effect during CPB, but the mechanism was unclear. So, we design this study to investigate the effects of EAc on CPB-induced lung injury and the underlying mechanism. Male Sprague Dawley rats were randomly divided into control, CPB, and CPB + EAc groups. A lung injury model was created by CPB surgery to serve as the CPB group, and EAc (2/100 Hz) was used before CPB in the CPB + EAc group. Lung tissue was collected at 0.5, 1, and 2 h after CPB. Pulmonary malondialdehyde (MDA) concentrations as well as superoxide dismutase (SOD), myeloperoxidase (MPO), and caspase-3 activity were determined. c-Jun N-terminal kinase (JNK), ERK, p38 and cleaved caspase 3 in the lung were analyzed by western blotting. A549 cells were treated by rat serum from the CPB and CPB + EAc groups, and cleaved caspase-3 activity was detected by fluorescent immunohistochemistry. CPB significantly increased the MPO activity, MDA content, apoptosis, caspase-3 activity, and phosphorylated p38 but decreased SOD activity compared with the control group. EAc significantly increased SOD activity at 0.5 and 2 h (p < 0.01 vs CPB) and reduced CPB-induced histological changes, MPO activity at 1 and 2 h (p < 0.05 vs CPB), MDA content at 2 h (p < 0.05 vs CPB), caspase-3 activity at 1 h (p < 0.05 vs CPB), and phosphorylated p38 and JNK at 0.5 h after CPB. The serum from the CPB group increased more positive staining cells of cleaved caspase-3 than that from the CPB + EAc group. EAc reversed the CPB-induced lung inflammation, oxidative damage, and apoptosis; the mechanism may involve decreased phosphorylation of p38 along with caspase-3 activity and activation.
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