Yamamoto M, Sakamoto N, Iwai A
Central Research Laboratories, Yamanouchi Pharmaceutical Co., Ltd., Ibaraki, Japan.
Arch Int Pharmacodyn Ther. 1990 Nov-Dec;308:178-84.
The effects of YM737, a glutathione analogue, and glutathione on neurological deficits and cerebral malondialdehyde concentrations were investigated in rats with experimental hematoma. A unilateral cerebral hematoma was provoked by injecting 0.25 ml of autologous blood around the capsula interna, putamen and caudate nucleus of the left cerebral hemisphere of the rat. Drugs were administered daily for four days beginning immediately after the operation. Neurological deficits and cerebral malondialdehyde concentrations were measured daily for 4 days. In the vehicle-treated group, deficits reached a maximum on the second day after the operation and then gradually recovered. YM737 (300 mg/kg, i.p.) accelerated recovery from neurological deficits, while glutathione had no effect. YM737 (300 mg/kg, i.p., on the fourth day after the operation) reduced the increase in malondialdehyde concentrations. Our results suggest that YM737 improves neurological deficits in this cerebral hematoma model, presumably partly due to inhibition of the lipid peroxidase response.
在实验性血肿大鼠中研究了谷胱甘肽类似物YM737和谷胱甘肽对神经功能缺损及脑丙二醛浓度的影响。通过在大鼠左脑半球内囊、壳核和尾状核周围注射0.25 ml自体血诱发单侧脑血肿。术后立即开始连续四天每日给药。连续4天每日测量神经功能缺损和脑丙二醛浓度。在溶剂处理组中，缺损在术后第二天达到最大值，然后逐渐恢复。YM737（300 mg/kg，腹腔注射）加速了神经功能缺损的恢复，而谷胱甘肽则无作用。YM737（300 mg/kg，腹腔注射，在术后第四天）降低了丙二醛浓度的升高。我们的结果表明，YM737改善了该脑血肿模型中的神经功能缺损，推测部分原因是抑制了脂质过氧化反应。
