BARBITURATE PROMOTES POSTISCHEMIC REAGGREGATION OF POLYRIBOSOMES IN GERBIL HIPPOCAMPUS

BARBITURATE PROMOTES POSTISCHEMIC REAGGREGATION OF POLYRIBOSOMES IN GERBIL HIPPOCAMPUS
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DOI:
10.1016/0304-3940(92)90176-8
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发表时间:
1992-10-26
影响因子:
2.5
通讯作者:
HOSSMANN, KA
HOSSMANN, KA
中科院分区:
医学4区
文献类型:
--
作者:
BONNEKOH, P;KUROIWA, T;HOSSMANN, KA

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短暂的脑缺血后会出现蛋白质合成的严重抑制,这种抑制在大脑的抵抗区域缓慢逆转,但在选择性脆弱的区域则不然。抑制发生在翻译水平,核糖体分解成单体就证明了这一点。为了评估这种干扰对缺血性损伤演变的重要性,在双侧颈动脉闭塞 5 分钟的沙鼠中研究了神经保护药物戊巴比妥对核糖体聚集的影响。缺血后不久应用戊巴比妥(50 mg/kg,腹腔注射),并在 15 分钟至 1 天的再循环时间后通过电子显微镜研究核糖体的聚集状态。戊巴比妥治疗并不能阻止最初的缺血后解聚,但促进了选择性脆弱神经元随后的重新聚集。这表明缺血后应用巴比妥类药物通过逆转脆弱区域缺血后核糖体重新聚集的阻滞而发挥其有益作用。
A brief period of cerebral ischemia is followed by severe inhibition of protein synthesis which is slowly reversed in the resistant but not in the selectively vulnerable regions of the brain. Inhibition occurs at the translational level, as evidenced by the disaggregation of ribosomes into monosomes. In order to evaluate the importance of this disturbance for the evolution of ischemic injury, the effect of the neuroprotective drug, pentobarbital, on ribosomal aggregation was studied in gerbils subjected to 5 min bilateral carotid artery occlusion. Pentobarbital (50 mg/kg, i.p.) was applied shortly after the ischemia, and the aggregational state of ribosomes was investigated by electron microscopy after recirculation times ranging from 15 min to 1 day. Pentobarbital treatment did not prevent the initial post-ischemic disaggregation but promoted the subsequent reaggregation in the selectively vulnerable neurons. This suggests that post-ischemic application of barbiturates exerts its beneficial effect by reversing the post-ischemic block of ribosomal reaggregation in vulnerable regions.