Abstract
Objective To evaluate the effect of propofol on brain injury during hepatic ischemia-reperfusion (I/R) in preadolescent mice. Methods Forty-eight healthy male C57BL/6 mice, aged 2 weeks, weighing 6-9 g, were allocated to one of 3 groups (n=16 each) using a random number table: sham operation group (group S), hepatic I/R group (group I/R) and propofol group (group P). Hepatic I/R was produced by occlusion of the blood supply to the median and left lobes of the liver for 60 min followed by reperfusion in anesthetized mice.In group P, 1% propofol 30 mg/kg was intraperitoneally injected at 30 min before skin incision, while the equal volume of normal saline was given instead in S and I/R groups.Blood samples were collected and brains were removed at 24 h of reperfusion, and hippocampi were then isolated.The levels of tumor necrosis factor-alpha (TNF-α) and interleukin-1beta (IL-1β) in hippocampi and levels of TNF-α, IL-1β, S-100β protein and neuron-specific enolase (NSE) in serum were determined by enzyme-linked immunosorbent assay.The pathological changes of hippocampi were examined with a light microscope, the apoptosis in hippocampal cells was measured using TUNEL, and the apoptotic index was calculated. Results Compared with group S, the TNF-α and IL-1β levels in serum and hippocampi, levels of S-100β protein and NSE in serum and apoptotic index were significantly increased (P<0.01), and the pathological changes of hippocampi were aggravated in I/R and P groups.Compared with group I/R, the TNF-α and IL-1β levels in serum and hippocampi, levels of S-100β protein and NSE in serum and apoptotic index were significantly decreased (P<0.05), and the pathological changes of hippocampi were attenuated in group P. Conclusion Propofol reduces brain injury induced by hepatic I/R, and the mechanism may be related to inhibition of systemic and central inflammatory responses of preadolescent mice. Key words: Propofol; Liver; Reperfusion injury; Brain
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