清开灵对大鼠谷氨酸神经毒性脑水肿时突触体游离钙的影响

Effects of Qingkailing on Free Calcium of Synaptosomes in Rats with Neurotoxic Brain Edema Induced by L-glutamate

摘要:

目的 探讨清开灵注射液对谷氨酸(Glu)神经毒性脑水肿时突触体内游离钙(［Ca2+］i)的影响。方法 30只大鼠分成正常对照组、模型组、治疗组3组，右侧脑室注射Glu制作大鼠神经毒性脑水肿模型，4 h后处死大鼠测定其脑皮质含水量、钠、钾、钙和突触体［Ca2+］i含量。结果 模型组脑含水量(82.04±0.8)%，钠含量(244.4±29.3) mmol/kg，［Ca2+］i (327.9±33.2) nmol/L分别较正常对照组(79.93±0.59)%，(213.8±13.0) mmol/kg，(159.6±18.6) nmol/L显著升高(P<0.01，P<0.05，P<0.01)，模型组钙(4.76±0.74) mmol/kg较正常对照组(5.21±0.81) mmol/kg显著降低(P<0.05)。治疗组脑含水量(80.13±0.72)%，钠含量(209.4±14.7) mmol/kg，［Ca2+］i (162.5±17.6) nmol/L较模型组显著降低(P均<0.01)，钙(5.44±0.76 mmol/kg.干重)却增高(P<0.05)。结论 清开灵对大鼠谷氨酸神经毒性脑水肿有保护作用，其机制可能与拮抗突触体钙离子内流有关。

Abstract:

Objective To determine the effects ofQingkailing Injection (QKL) on free calcium of synaptosomes in rats with neuroto xic brain edema (NBE) induced by L-glutamate. Methods Thirty S pragueDawley rats were randomly divided into 3 groups: ①sham control group (SHA, n=10); ②model group (MOD, n=10); ③therapy group (QKL, n=10), each rat was injected QKL (10 ml/kg, i.p.). The water content and the concentrations of sodiu m, potossium, calcium of the cerebral cortex and free calcium (［Ca2+］i) of the synaptosomes were determined at 4 hours after injecting chloride sodium o r glutamate into the right lateral ventricle. Results The level of water content 82.04%±0.8%, and the concentrations of sodium (244. 4±29.3) mmol/kg and ［Ca2+］i (327.9±33.2) nmol/L signific antly increased in MOD compared with SHA 79.93%±0.59%, (213.8±13 .0) mmol/kg, (159.6±18.6) nmol/L,P<0.01, P<0.05, P<0.01 respectively, while the concentraion of calcium in MOD (4.76± 0.74) mmol/kg significantly decreased compared with SHA (5.21±0.81) m mol/kg (P<0.05). The water content 80.13%±0.72% and the concent rations of sodium (209.4±14.7) mmol/kg and ［Ca2+］i (162.5± 17.6) nmol/L significantly decreased in QKL compared with MOD (P<0.01, 0.01, 0.01 respectively), while calcium (5.44±0.76) mmol/kg increased (P<0.05). Conclusions These findings suggest that QKL can protect against NBE, whose mechanism may be related to preventing the free calcium of the synaptosomes influx.