This study investigated whether propofol protects against endotoxin-induced myocardial injury by inhibiting NF-κB-mediated inflammation. Thirty clean male SD rats were randomly divided into a control (n=10), a model (n=10) and a propofol group (n=10). The model and propofol groups were injected with lipopolysaccharide (LPS) via the caudal vein to establish animal models of myocardial injury. At the same time, the control group was injected with normal saline via the caudal vein. At 30 min after the injections, the propofol group was treated with a continuous intravenous infusion of propofol, the control and model groups were injected with normal saline, and the three groups were treated continuously for 4 h. The changes in levels of interleukin-1 (IL-1), interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α) in serum were detected via enzyme-linked immunosorbent assay (ELISA). The mRNA expression level of nuclear factor-κB (NF-κB) in myocardial tissues was detected via quantitative real-time polymerase chain reaction (qRT-PCR). The protein expression levels of NF-κB, Bax and Bcl-2 in atrial muscles in each group were measured via Western blotting. The damage of myocardial tissues was detected via hematoxylin eosin (H&E) staining of tissues. Our results showed that compared with those in control group, the levels of IL-1, IL-6 and TNF-α in serum in the model and propofol groups were significantly higher; however, the levels in the model group, were significantly higher than those in the propofol group (P<0.01). The mRNA and protein expression levels of NF-κB in the propofol group were significantly lower than those in the model group (P<0.01). Likewise, the protein expression levels of Bax were significantly lower, while those of Bcl-2 were significantly increased. H&E staining showed that the myocardial tissues in the model group were damaged significantly, but the damage in the propofol group was significantly less severe. Based on our findings, it seems propofol can indeed protect against endotoxin-induced myocardial injury through its inhibition of the NF-κB-mediated inflammatory pathway.

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