Lima Juliana B M, Veloso Clarice C, Vilela Fabiana C, Giusti-Paiva Alexandre
Department of Physiology, Ribeirão Preto School of Medicine, University of São Paulo, Ribeirão Preto, Brazil.
Laboratory of Translational Physiology, Department of Physiological Sciences, Institute of Biomedical Sciences, Federal University of Alfenas-MG, Av. Jovino Fernandes Sales, 2600 Prédio E, Sala 300, 37130-000, Alfenas, MG, Brazil.
J Physiol Sci. 2017 Nov;67(6):673-679. doi: 10.1007/s12576-016-0494-8. Epub 2016 Oct 3.
Previous studies have demonstrated that zymosan, a cell wall component of the yeast Saccharomyces cerevisiae, induces inflammation in experimental models. However, few studies have evaluated the potential of zymosan to induce sickness behavior, a central motivational state that allows an organism to cope with infection. To determine whether zymosan administration results in sickness behavior, mice were submitted to the forced swim (FST) and open field (OFT) tests 2, 6, and 24 h after treatment with zymosan (1, 10, or 100 mg/kg). Additionally, to evaluate the possible relationship between zymosan-induced sickness behavior and prostaglandin synthesis, mice were pretreated with the cyclooxygenase inhibitors indomethacin (10 mg/kg) and nimesulide (5 mg/kg) and the glucocorticoid drug dexamethasone (1 mg/kg). Zymosan induced time-dependent decreases in locomotor activity in the OFT, and an increase in immobility in the FST, and increased plasma levels of corticosterone at 2 h. Pretreatment with indomethacin, nimesulide, or dexamethasone blocked zymosan-induced behavioral changes in both the FST and OFT at 2 h post administration. These findings confirm previous observations that zymosan induces sickness behavior. Furthermore, our results provide new evidence that prostaglandin synthesis is necessary for this effect, as anti-inflammatory drugs that inhibit prostaglandin synthesis attenuated zymosan-induced behavioral changes.
先前的研究表明，酵母聚糖（酿酒酵母的一种细胞壁成分）可在实验模型中诱发炎症。然而，很少有研究评估酵母聚糖诱发疾病行为的可能性，疾病行为是一种核心动机状态，使生物体能够应对感染。为了确定给予酵母聚糖是否会导致疾病行为，在用酵母聚糖（1、10或100mg/kg）治疗后2、6和24小时，对小鼠进行强迫游泳（FST）和旷场（OFT）试验。此外，为了评估酵母聚糖诱发的疾病行为与前列腺素合成之间的可能关系，用环氧化酶抑制剂吲哚美辛（10mg/kg）、尼美舒利（5mg/kg）和糖皮质激素药物地塞米松（1mg/kg）对小鼠进行预处理。酵母聚糖导致OFT中运动活动随时间减少，FST中不动时间增加，并在2小时时使血浆皮质酮水平升高。在给药后2小时，用吲哚美辛、尼美舒利或地塞米松预处理可阻断酵母聚糖在FST和OFT中诱发的行为变化。这些发现证实了先前的观察结果，即酵母聚糖可诱发疾病行为。此外，我们的结果提供了新的证据，表明前列腺素合成对于这种效应是必要的，因为抑制前列腺素合成的抗炎药物可减轻酵母聚糖诱发的行为变化。
