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首页> 外文期刊>Cytokine >Parthenolide attenuates LPS-induced fever, circulating cytokines and markers of brain inflammation in rats.
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Parthenolide attenuates LPS-induced fever, circulating cytokines and markers of brain inflammation in rats.

机译：爬山虎酚可减轻LPS引起的发热，循环细胞因子和大鼠脑部炎症的标志物。

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Parthenolide, a sesquiterpene lactone, has been reported to exhibit a variety of anti-inflammatory and immunomodulatory effects. To test the effect of parthenolide on brain inflammatory responses, brain oxidative stress and fever, we treated rats with parthenolide (1 mg/kg), simultaneously or 1 h prior to a systemic (i.p.) challenge with a moderate dose (100 mug/kg) of lipopolysaccharide (LPS). The initial hypothermia was exaggerated; the second phase of the biphasic LPS-induced fever and circulating interleukin-6 (IL-6) and tumor necrosis factor alpha (TNFalpha) were significantly attenuated only in parthenolide-pretreated animals. In the hypothalamus, markers of NFkappaB/NF-IL6 pathway activation (inhibitor kappaBalpha, NF-IL6 and the serin/threonin kinase-like protein mRNA expression) and markers of oxidative stress (including nuclear respiratory factor 1) and NFkappaB immunoreactivity were significantly reduced while NF-IL6 immunoreactivity and suppressor of cytokine signaling 3 mRNA expression remained unaltered, 8 h after LPS-stimulation with parthenolide-pretreatment. Importantly, this response was accompanied by decreased mRNA expression of the rate limiting enzyme in prostaglandin synthesis, cyclooxygenase 2 (COX2), known for its critical role in fever induction pathways. A direct action of parthenolide on brain cells was also confirmed in a primary neuro-glial cell culture of the vascular organ of the lamina terminalis a pivotal brain structure for fever manifestation with a leaky blood-brain barrier. In summary, pretreatment with parthenolide attenuates the febrile response during LPS-induced systemic inflammation by reducing circulating IL-6 and TNFalpha and decreasing hypothalamic NFkappaB/NF-IL6 activation, oxidative stress and expression of COX2. Thus parthenolide appears to have the potential to reduce brain inflammation.
机译：据报道，倍半萜内酯是倍半萜内酯，具有多种抗炎和免疫调节作用。为了测试小白菊内酯对脑部炎症反应，脑部氧化应激和发烧的影响，我们在中度剂量（100杯/千克）全身性（ip）攻击之前或同时1小时用小白菊内酯（1 mg / kg）治疗大鼠脂多糖（LPS）。最初的体温过高被夸大了; LPS诱导的发烧和循环白细胞介素6（IL-6）和肿瘤坏死因子α（TNFalpha）的第二阶段仅在用小白菊内酯预处理的动物中显着减弱。在下丘脑中，NFkappaB / NF-IL6途径激活的标志物（抑制剂kappaBalpha，NF-IL6和丝氨酸/苏氨酸激酶样蛋白mRNA表达）和氧化应激的标志物（包括核呼吸因子1）和NFkappaB免疫反应性显着降低LPS刺激和小白菊内酯预处理后8 h，NF-IL6免疫反应性和细胞因子信号转导抑制因子3 mRNA表达仍未改变。重要的是，该反应伴随着前列腺素合成中环氧酶2（COX2）中限速酶的mRNA表达下降，而环氧酶2在发烧诱导途径中起关键作用。在层板末端血管器官的原代神经胶质细胞培养物中，也证实了单酚对脑细胞的直接作用，这是发烧表现的关键性大脑结构，具有血脑屏障渗漏。总之，用小白菊内酯预处理可通过减少循环中的IL-6和TNFalpha并降低下丘脑NFkappaB / NF-IL6活化，氧化应激和COX2的表达来减轻LPS诱导的全身性炎症期间的发热反应。因此，小白菊内酯似乎具有减轻脑部炎症的潜力。

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