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首页> 外文期刊>Cell and Tissue Research >STAT3 and COX-2 activation in the guinea-pig brain during fever induced by the Toll-like receptor-3 agonist polyinosinic:polycytidylic acid
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STAT3 and COX-2 activation in the guinea-pig brain during fever induced by the Toll-like receptor-3 agonist polyinosinic:polycytidylic acid

机译：Toll样受体3激动剂多肌苷酸：聚胞苷酸在发烧期间豚鼠大脑中的STAT3和COX-2活化

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Intra-arterial injections of synthetic double-stranded RNA (polyinosinic:polycytidylic acid, PIPC) at a dose of 500 μg/kg evoked pronounced fever in guinea-pigs. PIPC-induced fever could be antagonized by treatment with the non-selective cyclooxygenase (COX) inhibitor diclofenac and was, in part, attenuated by the administration of the selective COX-2-inhibitor nimesulide (dose: 5 mg/kg for both COX inhibitors). We further investigated whether direct activation of brain cells during PIPC-induced fever could be demonstrated. Using radioactive in situ hybridization, we demonstrated that treatment with PIPC resulted in an upregulation of COX-2 and interleukin-1β mRNA in the guinea-pig brain. Thus, COX-2-specific hybridization signals seemed to be mainly associated with brain blood vessels. Intra-arterial injections of PIPC further induced the pronounced nuclear translocation of the transcription factor STAT3 in the endothelium of various fore- and hindbrain areas and in the meninges. In brain structures that lacked a tight blood-brain barrier, i.e. the sensory circumventricular organs (area postrema, vascular organ of laminae terminalis, subfornical organ), the astrocytes and a population of still undetermined cellular phenotype also showed marked STAT3 activation in response to PIPC. The Toll-like receptor-3 agonist PIPC therefore caused a similar activation of brain cells as that reported for other experimental models of systemic inflammation.
机译：动脉内注射500μg/ kg合成双链RNA（polyinosinic：polycytidylic acid，PIPC）在豚鼠中引起明显发热。 PIPC引起的发烧可以通过使用非选择性环氧化酶（COX）抑制剂双氯芬酸来拮抗，并且通过施用选择性COX-2抑制剂尼美舒利（部分剂量：两种COX抑制剂为5 mg / kg）可以部分减轻）。我们进一步调查了是否可以证明PIPC引起的发烧期间脑细胞的直接激活。使用放射性原位杂交，我们证明用PIPC治疗导致豚鼠脑中COX-2和白介素1βmRNA的上调。因此，COX-2特异性杂交信号似乎主要与脑血管有关。 PIPC的动脉内注射进一步在各个前脑和后脑区域的内皮以及脑膜中诱导了转录因子STAT3的明显核易位。在缺乏紧密的血脑屏障的大脑结构中，即感觉性脑室室器官（区域的后部，椎板的终末血管器官，子宫颈下器官），星形胶质细胞和仍未确定的细胞表型群体也显示出对PIPC的显着STAT3活化作用。 。因此，Toll样受体3激动剂PIPC引起了与其他全身性炎症实验模型报道的大脑细胞类似的激活。

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