Abstract

Objective To investigate the effects of cardiopulmonary bypass (CPB) on vascular endothelial inflammation and oxidative stress in rats and its mechanism. Methods 64 SD male rats were randomly divided into sham group and CPB group, and the CPB rat model was prepared. The vascular endothelial function was compared after 4 hours of CPB. tumor necrosis factor-α (TNF-α), interleukin (IL)-1β and IL-6 was detected by enzyme linked immunosorbent assay (ELISA). The serum levels of malondialdehyde (MDA), superoxide dismutase (SOD) and glutathione (GSH) was analyzed using MDA, SOD and GSH test kit. The protein activity of nuclear factor-κB (NF-κB) in aorta was detected by Western blotting. Results Compared with the sham group [(90.17±7.45)%], the diastolicity of aortic vascular in CPB group was significantly decreased [(72.57±5.86)%, t=2.869, P<0.05]. Compared with the sham group [(118.53±9.70), (87.69±10.46), (91.88±10.04) ng/L], the serum levels of TNF-α, IL-6 and IL-1β in the CPB group increased significantly [(203.55±13.29), (170.20±11.81), (176.49±16.11) ng/L] (t=3.347, 4.253, 3.850, P<0.05). Compared with the sham group [(67.38±7.17) U/ml; (21.04±3.7) μmol/L; (20.33±1.79) mg/L] the serum levels of SOD and GSH in the CPB group were significantly decreased, while the serum level of MDA was significantly increased [(40.38±5.21) U/ml; (34.04±5.0) μmol/L; (13.86±1.51) mg/L, t=2.772, 2.397, 3.216, P<0.05]. Western blotting showed that compared with the sham group (0.62±0.04), the relative expression of phospho-NF-κB p65 in the aorta tissue of the CPB group was significantly increased (1.44±0.12, t= 3.750, P<0.05). Conclusion CPB can inhibit vascular endothelial function in rats by enhancing vascular endothelial inflammation and oxidative stress levels. Key words: Cardiopulmonary bypass; Vascular endothelial; Inflammation; Oxidative stress; Nuclear factor-κB

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call

Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.