Protective effect of hyperbaric oxygen on cardiac function in rats with acute myocardial infarction by regulating inflammatory response and cell apoptosis

Abstract

Objective To investigate the role of hyperbaric oxygen (HBO) in the regulation of inflammatory response and myocardial cell apoptosis in the process of alleviating myocardial infarction in rats. Methods Thirty 4-week SD rats were randomly divided into 3 groups, i. e. the sham surgery group, the model group and the HBO oxygen group. Acute myocardial infarction (AMI) model was established by coronary artery ligation. Left ventricular ejection fraction (EF), short-axis contraction (FS) and changes in maximum systolic and diastolic pressure (±dp/dtmax) were measured by echocardiography and hemodynamics. The expression levels of inflammatory factors in serum and cardiac muscle tissues of each group were detected by ELISA and qRT-PCR. Western blotting was used to detect the expression levels of apoptosis-related proteins in myocardial tissues of each group. Results As compared with those of the sham surgery group, the EF and FS of the model group significantly decreased and the absolute value of ± dp/dtmax was significantly down-regulated (P<0.01). Following HBO treatment, the EF, FS and ± dp/dtmax were all significantly higher than those of the model group (P<0.05). The expression levels of IL-6, IL-1β, TNF-α and CRP in the serum inflammatory factors of the model group were significantly up-regulated (P<0.05). After HBO treatment, the expression levels of the IL-1β, IL-6, TNF-α and CRP in the serum inflammatory factors of the HBO group were all lower than those of the model group (P<0.05). The expression levels of IL-1β, IL-6, TNF-α mRNA in the myocardial tissue were all significantly higher than those of the control group (P<0.01). Following HBO treatment, the expression levels of IL-1β, IL-6, TNF-α mRNA in the myocardial tissue of the AMI rats were significantly down-regulated, as compared with those of the model group (P<0.05). The expression levels of bax and c-caspase-3 in the model group were up-regulated, as compared with those of the sham surgical group, while the expression level of Bcl-2 was down-regulated (P<0.05). As compared with the model group, HBO treatment could significantly down-regulate the expression levels of bax and c-caspase-3, and in the meantime up-regulate the expression level of Bcl-2(P<0.05). Conclusion HBO treatment could significantly decrease inflammatory response and apoptosis of cardiocytes in the rats with AMI, thus alleviating symptoms of AMI. Key words: Hyperbaric oxygen; Acute myocardial infarction; Inflammatory response; Apoptosis