丁基苯酞对局部脑缺血大鼠神经元迟发性损伤及细胞内钙的影响

观察了丁基苯酞(NBP)对局部脑缺血迟发性脑梗塞和神经功能缺损的影响。结果表明,大鼠大脑中动脉阻断(MCAO)后2h分别poNBP80,160和240mg·kg^-1,均能明显降低脑梗塞面积,抑制率分别为49.0%,69.5%及85.1%,并明显改善神经功能缺失。在MCAO前1h予防给NBP(160mg·kg^-1po),也可明显缩小脑梗塞面积和改善神经功能缺失;在MCAO前连续口服7d,NBP剂量为80mg·kg^-1·d^-1,对上述指标均有改善作用。NBP对高K⁺引起大鼠脑突触体内Ca²⁺含量升高无影响。以上结果提示NBP对迟发性神经元损伤有保护作用。

EFFECT OF DL-3-N-BUTYLPHTHALIDE ON DELAYED NEURONAL DAMAGE AFTER FOCAL CEREBRAL ISCHEMIA AND INTRASYNAPTOSOMES CALCIUM IN RATS

Effect of dl-3-n-butylphthalide on the size of infarction and behavior changes wereinvestiga ted a fter delayed neuronal damage in rats s ubjected to permane nt middle cerebral artervocclusion(MCAo)by the methed of Tamura et al. and the scores of behavior were evaluated by themethed of Bederson et al, The results show that the size of infarct area was significantly reduced 2hafter MCAO following administration of NBP at the dose of 80,160 and 240 mg· kg^-1 ,thepercentage of reduction of infarct area was 49.0%, 69.5%and 85.1%respectively. Neurologicaldeficit was also improved. The size of infarction and the score of neurological deficit were also reducedsignificantly following pretreatment with NBP at the dose of 80 mg·kg^-1 per day for 7 days by theend of the final dosage 24 h before MCAO or at the single dose of l60 mg·kg^-1 1h before MCAO.The results suggest that NBP has therapeutic and preventive effect on stroke and imply that NBP hasthe action of attenuating neuronal damage after delayed cerebral injury. In addition , the level ofcalcium(Ca²⁺]i) in rat intrasynaptosomes was determined using fura-2(a fluorescence indicator)technique. It was found that NBP ean not lower the rise ofCa²⁺]i induced by 30 mmol·L^-1 KCl,However, the effect of NBP on Ca²⁺]i overload induced by excitatory amino acid remains to bestudied.