清开灵对家兔内毒素性发热的作用及机制研究

目的:探讨清开灵(QKL)注射液对家兔内毒素性发热的解热作用和机制。方法:复制家兔内毒素(ET)性发热模型, 用数字温度计测量家兔的直肠温度, 用放免法测定下丘脑的IL-1β和cAMP、脑脊液中的cAMP、腹中隔区的AVP含量。结果:QKL+ET组的△T(0.24±0.10)℃、TRI₁(1.02±0.81)、下丘脑IL-1β(3.02±0.58)ng/g、下丘脑cAMP(1.37±0.23)nmol/g、CSF中cAMP(14.13±3.80)nmol/L、腹中隔区AVP(25.24±2.61)ng/g, 分别低于ET组的△T(0.40±0.11)℃、TRI₁(1.78±0.79)、下丘脑IL-1β(6.08±0.79)ng/g、下丘脑cAMP(2.90±0.40)nmol/g、CSF中cAMP(32.10±4.51)nmol/L、腹中隔区AVP(47.32±3.77)ng/g, 两者相比差异显著(P<0.01)。结论:QKL抑制下丘脑内生致热原和中枢发热介质的生成, 促进解热物质的释放, 可能是QKL对内毒素性发热的重要解热机制。

Effect and mechanism of Qing-Kai-Ling on endotoxin-induced fever in rabbits

AIM:To explore the antipyretic mechanism of Qing Kai-Ling (QKL) injection on endotoxin (ET)-induced fever in rabbits.METHODS:Rabbit models of endotoxin (ET)-induced fever were duplicated. The rectal temperature was measured by digital thermograph. The cAMP and IL-1β content in the hypothalamus (HP), the cAMP content in the cerebrospinal fluid (CSF), and the arginine vasopressin (AVP) content in the ventral septal area (VSA) were determined by radioimmunoassay.RESULTS:① QKL had significant antipyretic effect on ET-induced fever(P<0.01), ② The production of IL-1β and cAMP in HP was significantly inhibited by QKL treatment (P<0.01), ③ QKL markedly decreased the cAMP content in the CSF and AVP content in the VSA(P<0.01).CONCLUSION:The antipyretic mechanisms of QKL are probably due to inhibiting the production of the endogenous pyrogen and central mediator of fever, and meanwhile stimulating the release of the antipyretic substances.