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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.