首页> 外文期刊>Bulletin of experimental biology and medicine >Dipeptide analog of neurotensin active site prevents the development of experimental Parkinson's syndrome in mice.
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Dipeptide analog of neurotensin active site prevents the development of experimental Parkinson's syndrome in mice.

机译:神经降压素活性位点的二肽类似物可防止小鼠实验性帕金森综合症的发展。

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摘要

Chronic administration of neurotoxin 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (30 mg/kg) to C57BL/6 mice caused death of all animals within 7 days. Dipeptide analog of neurotensin active site injected with this neurotoxin protected the mice from death even after 2-week intoxication. When younger mice and lower dose of neurotoxin (25 mg/kg) were used, all animals survived, but after 2 weeks they developed parkinsonian syndrome with muscular rigidity, akinesia, decrease in motor and explorative activities. In mice treated with dipeptide analog of neurotensin active site these manifestations of oligokinesia caused by 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine were less pronounced and the corresponding parameters approximated the control values. Possible mechanisms of neuroprotective action of neurotensin active site analog are discussed.
机译:向C57BL / 6小鼠长期服用神经毒素1-甲基-4-苯基-1,2,3,6-四氢吡啶(30 mg / kg)导致7天内所有动物死亡。注射这种神经毒素的神经降压素活性位点的二肽类似物即使在中毒2周后仍能保护小鼠免于死亡。当使用较年轻的小鼠和较低剂量的神经毒素(25 mg / kg)时,所有动物均存活,但在2周后,他们发展出帕金森氏综合症,具有肌肉僵硬,运动障碍,运动和探索活动减少。在用神经降压素活性位点的二肽类似物治疗的小鼠中,这些由1-甲基-4-苯基-1,2,3,6-四氢吡啶引起的少肌反应的表现不太明显,并且相应的参数接近对照值。讨论了神经降压素活性位点类似物的神经保护作用的可能机制。

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