Protective Effects of Acupuncture in Cardiopulmonary Bypass-Induced Lung Injury in Rats.

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.