银杏类黄酮对大鼠脑损伤后机能改变的影响

EFFECTS OF FLAVONOID OF GINKGO BILOBA ON THE FUNCTIONAL CHANGES FOLLOWING BRAIN INJURY IN RATS

观测了银杏类黄酮 (flavonoidofGinkgobiloba ,FGb)对损伤大鼠运动皮层后机能改变过程的影响。结果表明 :(1)FGb明显促进运动平衡能力的恢复 ;(2 )损伤后脑室水肿明显 ,FGb促进脑水肿症状的恢复 ;(3)挫伤 3h后脑内的游离氨基酸递质水平明显下降 ,FGb促进脑内氨基酸水平的恢复。这可能是银杏叶提取物促进脑损伤修复的机制之一。

We used a modified animal model to evaluate the effects of flavonoid of Ginkgo biloba (FGb),a major content of extract of Ginkgo biloba (EGB), on the functional and physiological changes following traumatic brain injury(TBI). The cortical injury was impact delivered by a metal rod on the left motor cortex of the anesthetized rat. The impact device consists of a glass tube set vertically over the anesthetized rat head. A rod weighted 37 5 g with the diameter of its impact tip being 3 6 mm. Without destroying the dura, this impact injured the left motor cortex but did not produce significant cardio respiratory effects. Thus, neither generalized hypoxia, ischemia, nor brain herniation at the injured site with local ischmia hypoxia, confounded our conclusions. Male Wistar rats, weighting 150～200 g, were used in the three groups of experiments. In behavioral group, effects of FGb on the recovery process of locomotive equilibrium ability of rats following TBI were tested. A rotating beam was used to evaluate the locomotive equilibrium ability of the rats. Animals were randomly divided into three subgroups after cortex injury: (1) FGb treatment group ( n =4); (2) EGb treatment group ( n =6); (3) control group ( n =6). In cortex group the volume of cortex and lateral ventricles of the rats were measured 30 days after TBI. Animals were divided into three subgroups: (1) sham group ( n =6) in which animals received a craniotomy but were not injured; (2) L saline group ( n =6) in which animals were injured and treated with saline; (3) L FGb group ( n =6) in which animals were injured and treated with L FGb. In amino acid group we measured the concentration of two excitatory amino acids (glutamate and aspartic acid) and two inhibitory amino acids (GABA and glycine) in the cortex and hippocampus of rats at 3, 6 and 48 hour after TBI. Animals were divided into four subgroups: (1) normal group ( n =4) in which animals were sacrificed without craniotomy; (2)control group ( n =18) in which animals were injured and treated with saline; (3) FGb treatment group 1 ( n =18) in which animals were injured and treated with 25 mg/kg/d of FGb; (4) FGb treatment group 2 ( n =6) in which animals were injured and treated with 50 mg/kg/d of FGb. We found that FGb remarkably accelerated the recovery process of the locomotive equilibrium ability of rats after TBI and ameliorated cerebral edema caused by the injury. At 3 hours after injury, the concentrations of all four amino acids decreased. The duration and magnitude of the variation of the concentrations of these four amino acids were different between the cortex and hippocampus, and were also different with each other. But FGb obviously inhibited the immediate declination of those amino acids following the injury. These results indicate that the amelioration of edema and inhibition of the declination of the four amino acids following the injury may be the possible mechanisms of the promoting effects of FGb on the functional recovery of TBI.