Huang S S, Tsai S K, Chih C L, Chiang L Y, Hsieh H M, Teng C M, Tsai M C
Department of Pharmacology, College of Medicine, National Taiwan University, Taipei, Taiwan.
Free Radic Biol Med. 2001 Mar 15;30(6):643-9. doi: 10.1016/s0891-5849(00)00505-0.
The effects of hexasulfobutylated C60 (FC4S), a free radical remover, on the total volume infarct size elicited by the damaging effects of focal cerebral ischemia were studied on Long-Evans rats in vivo. FC4S was administered intravenously either 15 min before middle cerebral artery (MCA) occlusion (pretreatment groups) or it was injected when the common carotid arteries clips were removed (treatment groups). FC4S did not alter the pH, blood gases, heart rate, or mean arterial blood pressure in either pretreatment or treatment groups of the rats. However, after administration of FC4S at dosages of 10 and 100 microg/kg, the total volume of infarction was significantly reduced in both pretreatment and treatment groups. In addition, after FC4S administration, the nitric oxide (NO) content in plasma was increased and the lactate dehydrogenase (LDH) levels was decreased. It is concluded that FC4S may be used as a neuroprotective agent on focal cerebral ischemia. The beneficial effects may be partly related to its antioxidant property and to the upregulation of NO production of the compound.
在体内对Long-Evans大鼠研究了自由基清除剂六磺丁基化C60（FC4S）对局灶性脑缺血损伤所引发的梗死总体积大小的影响。在大脑中动脉（MCA）闭塞前15分钟静脉注射FC4S（预处理组），或者在移除颈总动脉夹时注射FC4S（治疗组）。FC4S在大鼠的预处理组或治疗组中均未改变pH值、血气、心率或平均动脉血压。然而，在以10和100微克/千克的剂量给予FC4S后，预处理组和治疗组的梗死总体积均显著减小。此外，给予FC4S后，血浆中一氧化氮（NO）含量增加，乳酸脱氢酶（LDH）水平降低。得出的结论是，FC4S可用作局灶性脑缺血的神经保护剂。其有益作用可能部分与其抗氧化特性以及该化合物一氧化氮生成的上调有关。
