摘要
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 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 80,16 0 and 24 0 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 of[Ca2+]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.
出处
《药学学报》
CAS
CSCD
北大核心
1996年第3期166-170,共5页
Acta Pharmaceutica Sinica
关键词
丁基苯酞
脑缺血
脑梗塞
神经功能缺失
dl-3-n-Butylphthalide
Middle cerebral artery occlusion
Cerebral infarct area:Neurological deficit
Intrasynaptosome calcium
