中风与神经疾病杂志
中風與神經疾病雜誌
중풍여신경질병잡지
JOURNAL OF APOPLEXY AND NERVOUS DISEASES
2001年
2期
87-88
,共2页
刘恒颖%康劲松%徐琪%郭中钰%祝世功
劉恆穎%康勁鬆%徐琪%郭中鈺%祝世功
류항영%강경송%서기%곽중옥%축세공
IL-1β缓慢释放颗粒人重组白细胞介素-1β%乙酰碱酯酶%脂质过氧化物%Meynert基底核
IL-1β緩慢釋放顆粒人重組白細胞介素-1β%乙酰堿酯酶%脂質過氧化物%Meynert基底覈
IL-1β완만석방과립인중조백세포개소-1β%을선감지매%지질과양화물%Meynert기저핵
目的探讨IL-1β对大鼠胆碱能神经元的损伤作用及机制。方法将IL-1β缓慢释放颗粒(IL-1β pellet)植入大鼠右侧Meynert核(nbM,基底核),复制胆碱能系统受损的动物模型;将不同剂量的人重组白细胞介素-1β(rhIL-1β)加入培养大鼠前脑基底神经元中,复制rhIL-1β诱导神经元损伤模型,检测(乙酰胆碱酯酶)AchE活性和脂质过氧化物(LPO)含量的变化。结果 IL-1β损伤侧皮质AchE活性较未损伤侧、正常组及假手术组均显著降低(P<0.01)。50-500U/ml rhIL-1β可引起培养的神经元AchE活性明显下降(P<0.05);100-500U/ml rhIL-1β可引起神经元LPO含量明显升高(P<0.01)。结论 IL-1β慢性作用可以造成大鼠中枢胆碱能系统的损害,其机制可能是通过脂质过氧化作用。
目的探討IL-1β對大鼠膽堿能神經元的損傷作用及機製。方法將IL-1β緩慢釋放顆粒(IL-1β pellet)植入大鼠右側Meynert覈(nbM,基底覈),複製膽堿能繫統受損的動物模型;將不同劑量的人重組白細胞介素-1β(rhIL-1β)加入培養大鼠前腦基底神經元中,複製rhIL-1β誘導神經元損傷模型,檢測(乙酰膽堿酯酶)AchE活性和脂質過氧化物(LPO)含量的變化。結果 IL-1β損傷側皮質AchE活性較未損傷側、正常組及假手術組均顯著降低(P<0.01)。50-500U/ml rhIL-1β可引起培養的神經元AchE活性明顯下降(P<0.05);100-500U/ml rhIL-1β可引起神經元LPO含量明顯升高(P<0.01)。結論 IL-1β慢性作用可以造成大鼠中樞膽堿能繫統的損害,其機製可能是通過脂質過氧化作用。
목적탐토IL-1β대대서담감능신경원적손상작용급궤제。방법장IL-1β완만석방과립(IL-1β pellet)식입대서우측Meynert핵(nbM,기저핵),복제담감능계통수손적동물모형;장불동제량적인중조백세포개소-1β(rhIL-1β)가입배양대서전뇌기저신경원중,복제rhIL-1β유도신경원손상모형,검측(을선담감지매)AchE활성화지질과양화물(LPO)함량적변화。결과 IL-1β손상측피질AchE활성교미손상측、정상조급가수술조균현저강저(P<0.01)。50-500U/ml rhIL-1β가인기배양적신경원AchE활성명현하강(P<0.05);100-500U/ml rhIL-1β가인기신경원LPO함량명현승고(P<0.01)。결론 IL-1β만성작용가이조성대서중추담감능계통적손해,기궤제가능시통과지질과양화작용。
Objective To observe the effect and mechanism of IL-1β on cholinergic neurons in the rat. Methods IL-1β pellet was put into right side of nucleus basalis of Meynert to make cholinergic system damaged. Different doses of rhIL-1β were added into cultured forebrain neurons to make cultured neuron damaged. AchE activity and lipid peroxide(LPO) content were measured respectively. Results In the rat model AchE acitivity in cerebral cortex was lowered significantly. In cultured neuron 50~500 U/ml doses of rhIL-1β reduced AchE acitivity and 100~500U/ml increased LPO content. Conclusion Chronic stimulation of interleukin-1 can damage central cholinergic neurons and its projectile system by one way of neuronal peroxidization.