α-MSH对EGTA发热的作用

The effect of α-MSH on EGTA-induced fever

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。

AIM: To investigate the effect of α-MSH on fever induced by EGTA and its possible mechanism.METHODS:EGTA evoked a rise in colonic temperature. The intracellular free calcium([Ca 2+ ] i) in isolated cells from hypothalamus was examined using spectrofluormetry with fura-2 and hypothalamic cells were cultured in vitro .RESULTS:α-MSH could markedly suppressed febrile response ( P<0.01 ). The level of [Ca 2+ ] i decreased while cells were exposed to medium containing EGTA ( P<0.01 ),but α-MSH had no effect on this decrease action ( P>0.05 ). The corticotropin releasing hormone (CRH) content of culture supernatant significantly elevated when hyperthermic cells were incubated in the presence of EGTA ( P<0.05 ).CONCLUSION:The effect of α-MSH preventing CRH production in the hypothalamus may play a main role in α-MSH antipyretic action and CRH may be an important factor in the mechanism of EGTA-induced fever.