发热2015教程文件.ppt

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发热2015教程文件.ppt

(一) 体温调节中枢 (Thermoregulation center) 正调节中枢 负调节中枢 视前区-下丘脑前部 (preoptic anterior hypothalamus, POAH) 发热 激活物 体温? 下丘脑体温 调节中枢 体温 调定点? 产EP 细胞 EP ? (二)致热信号传入中枢的途径 EP通过血脑屏障转运入脑 EP通过终板血管器作用于体温调节中枢 EP通过迷走神经向体温调节中枢传递发热信号 News in Physiological Sciences 1997,12:1~9 EP 巨噬细胞 巨噬细胞 POAH神经元 POAH神经元 第三脑室视上隐窝 视神经交叉 毛细血管 OVLT区 ? (三) 发热中枢调节介质 中枢发热正调节介质 前列腺素E (PGE) Na+/ Ca2+比值 促肾上腺皮质激素释放激素 (CRH) 环磷酸腺苷 (cAMP) 一氧化氮(NO) Fever is a common response to inflammation and infection. The mechanism involves prostaglandin E2?(PGE2)-EP3 receptor signaling in the hypothalamus, which raises the set point of hypothalamic thermostat for body temperature, but the lipid metabolic pathway for pyretic PGE2?production remains unknown.? ?To reveal the molecular basis of fever initiation, we examined lipopolysaccharides (LPS)-induced fever model in monoacylglycerol lipase (MGL)-deficient (Mgll?/?) mice. We find?MGL is a critical enzyme for fever, which functions independently of endocannabinoid signals. ?MGL-dependent hydrolysis of endocannabinoid 2-arachidonoylglycerol is necessary for pyretic PGE2?production in the hypothalamus.But hypothalamic PGE2?caused by RANKL-RANK signaling in females may involve MGL-independent mechanism(s) in part, which awaits further studies. Fever Is Mediated by Conversion of Endocannabinoid 2-Arachidonoylglycerol to Prostaglandin E2 PLOS ONE 2015.7.21 Glutathione deficiency attenuates endotoxic fever in rats Glutathione constitutes the first line of the cellular defence mechanism against oxidative stress, and according to published data it is required by a number of factors that are involved in fever mechanism. The aim of the present study was to investigate whether or not glutathione deficiency can modulate a course of the fever induced by endotoxin (LPS). CONCLUSION: Based on these data, we conclude that glutathione deficiency modifies the LPS-induced fever, in a TNF-α related manner. Int J Hypert

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