Propofol improves intestinal ischemia-reperfusion injury in rats through NF-κB pathway

M.-B. Wu, B. Ma, T.-X. Zhang, K. Zhao, S.-M. Cui, S.-C. He

Department of Anesthesiology, Jinan City People’s Hospital, Jinan, China. wumaobin03@163.com

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• Pharmacology

OBJECTIVE: The aim of this study was to investigate the effects of propofol on intestinal ischemia-reperfusion injury in rats through the nuclear factor-kappa B (NF-κB) pathway.

MATERIALS AND METHODS: A total of 24 Sprague-Dawley rats were selected and randomly divided into three groups, including sham operation group, ischemia group and propofol group. Rats in sham operation group were only treated with isolation of superior mesenteric artery, which was clipped for 1 h and reperfused for 2 h in ischemia group. Meanwhile, propofol (60 mg/kg) was injected into the femoral vein 1 h before ischemia in propofol group. TUNEL assay was performed to detect cell apoptosis of intestinal tissues. Real-time quantitative polymerase chain reaction (RT-qPCR) was conducted to measure the expression levels of malondialdehyde (MDA), superoxide dismutase (SOD), myeloperoxidase (MPO), caspase-3 and B-cell lymphoma-2 (Bcl-2) in rats of each group. Western blotting was utilized to detect the protein expression levels of NF-κB pathway related molecules, such as myeloid differential protein-88 (MyD88), v-rel avian reticuloendotheliosis viral oncogene homolog A (RelA) and NF-κB. Furthermore, changes in plasma cytokine levels were determined via enzyme-linked immunosorbent assay (ELISA).

RESULTS: The number of apoptotic cells in ischemia group was remarkably higher than that in sham operation group (p<0.05). However, it decreased notably in propofol group compared with ischemia group (p<0.05). In comparison with sham operation group, significantly up-regulated expression of caspase-3 and down-regulated expression of Bcl-2 were observed in the intestinal tissues of rats in ischemia group (p<0.05). Caspase-3 was lowly expressed, while Bcl-2 was highly expressed in the intestinal tissues of rats in propofol group compared with ischemia group (p<0.05). In addition, no statistically significant differences were observed in the expression level of SOD among sham operation group, ischemia group and propofol group (p>0.05). The expression levels of MDA and MPO were overtly higher in the intestinal tissues of rats in ischemia group than those in sham operation group and propofol group (p<0.05). Besides, the protein expression levels of MyD88, RelA and NF-κB in the intestinal tissues of rats in ischemia group were remarkably higher than those in sham operation group and propofol group (p<0.05). The activity of the NF-κB pathway in the intestinal tissues of rats in propofol group significantly declined compared with ischemia group (p<0.05). Moreover, compared with sham operation group, plasma levels of TNF-α, interleukin (IL)-2, IL-6 and IL-4 increased significantly in rats of ischemia group (p<0.05). However, they were markedly lower in propofol group than those in ischemia group (p<0.05).

CONCLUSIONS: Propofol protects rats from intestinal ischemia-reperfusion injury through the NF-κB pathway.

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