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目的：观察α－ＭＳＨ对ＥＧＴＡ发热反应的作用及其可能机制。方法：建立ＥＧＴＡ发热模型；在离体条件下，应用Ｆｕｒａ－２荧光指示剂测定细胞内Ｃａ２＋浓度（［Ｃａ２＋］ｉ）；体外培养下丘脑神经细胞。结果：α－ＭＳＨ能明显抑制ＥＧＴＡ性发热反应（Ｐ＜０．０１）；ＥＧＴＡ可以降低下丘脑神经细胞［Ｃａ２＋］ｉ水平（Ｐ＜０．０１），但α－ＭＳＨ不影响正常下丘脑神经细胞［Ｃａ２＋］ｉ及ＥＧＴＡ对下丘脑神经细胞［Ｃａ２＋］ｉ的作用（Ｐ＞０．０５）；ＥＧＴＡ可刺激体外培养的下丘脑神经细胞释放ＣＲＨ（Ｐ＜０．０５），而α－ＭＳＨ能抑制ＥＧＴＡ的这种作用（Ｐ＜０．０５）。结论：α－ＭＳＨ抑制中枢发热介质ＣＲＨ的产生可能是降低ＥＧＴＡ发热反应的主要机制之一；中枢ＣＲＨ的产生和释放增加可能是ＥＧＴＡ性发热的一个重要因素。
Objective: To observe the effect of α-MSH on febrile response to EGTA and its possible mechanism. Methods: The model of EGTA fever was established. In vitro, the intracellular Ca2 + concentration ([Ca2 +] i) was measured with Fura-2 fluorescent indicator. Hypothalamic neurons were cultured in vitro. Results: α-MSH could significantly inhibit the febrile response to EGTA (P <0.01); EGTA decreased the level of [Ca2 +] i in hypothalamic neurons (P <0.01), but α-MSH did not affect normal hypothalamic nerve The effect of [Ca2 +] i and EGTA on [Ca2 +] i in hypothalamus neurons (P> 0.05). EGTA stimulated the release of CRH from hypothalamic neurons in vitro (P <0.05) Can inhibit this effect of EGTA (P <0.05). CONCLUSION: Inhibition of α-MSH on the production of CRH in central nervous system may be one of the main mechanisms for reducing the febrile response to EGTA. Increased production and release of central CRH may be an important factor in EGTA-induced fever.