| 其他摘要 | The cytokines are synthesized and released in response to infection and inflammation, which could induce sickness behaviours in human beings as well as animals; however, the role of cytokines in the pathology of sickness behaviours is still not clear. The object of the thesis is to investigate the effects of the peripheral cytokines on sickness behaviours. The methods: The sickness behaviours were induced by lipopolysaccharide, a cytokine inducer, in rats. Before the injection of lipopolysaccharide, animals were pretreated with cholecystokinin octapeptide, an anti-inflammatory, or fluoxetine, one kind of antidepressants, to inhibit the release of proinflammatory cytokines. Following the injection, the effects of peripheral cytokines on the sickness behaviours and the change of the peripheral proinflammatory cytokines IL-1β, IL-6 and TNF-α and anti-inflammatory cytokine IL-10 were observed. This thesis included three experiments: 1) the effects of cholecystokinin octapeptide on the lipopolysaccharide-induced sickness behaviours and peripheral cytokines, 2) the effects of different doses of cholecystokinin octapeptide on the lipopolysaccharide-induced behaviours and peripheral cytokines, and 3) the effects of chronic and acute fluoxetine treatment on the lipopolysaccharide-induced behaviours and peripheral cytokines. Sickness behaviours were measured by using the sugar water consumption test, open field test and elevated plus maze after the injection, and cytokines in sera were analysed by immunoassays. The results: Lipopolysaccharide induced sickness behaviours and the release of cytokines including IL-1β, IL-6 and TNF-α in rats. The treatment of cholecystokinin octapeptide (20 μg/kg, 40 μg/kg, 80 μg/kg and 120 μg/kg, i.p., half hour before the injection of lipopolysaccharide) could abolish the lipopolysaccharide-induced release of cytokines (IL-1β、IL-6 and TNF-α), but this effect did not enhance when the dosage increased. Cholecystokinin octapeptide could not attenuate the lipopolysaccharide-induced sickness behaviours in all dosage. Both the chronic (15 days) and acute (half hour before the injection of lipopolysaccharide) fluoxetine (20 mg/kg, i.p.) treatment could not attenuate the lipopolysaccharide-induced sickness behaviours, though the acute fluoxetine treatment inhibited the lipopolysaccharide-induced cytokines (IL-1β、IL-6 and TNF-α), and the chronic fluoxetine treatment significantly inhibited TNF-α. It was also found that acute fluoxetine treatment per se increased peripheral IL-10 secretion while all other treatments have no effects on IL-10 secretion. These results suggested that the release of peripheral proinflammatory cytokines were involed in the development of sickness behaviours, but the inhibition of peripheral proinflammatory cytokines could not antagonize the sickness behaviours. |
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