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出 处:《药学学报》1994年第7期492-496,共5页Acta Pharmaceutica Sinica
摘 要:结果表明,粉防己碱(Tet)非常明显地阻断K+去极化导致的胎鼠大脑[Ca2+]i含量的增加。经不同浓度Tet处理的大脑细胞加入KCl后,[Ca2+]i含量仍基本维持在静息状态下水平。对[Ca2+]i的阻断程度与Tet浓度无关。Tet对L-谷氨酸(L-Glu)所致大脑[Ca2+]i升高亦有明显抑制作用。10-7mol·L-1浓度的Tet还降低BayK8644引起的[Ca2+]i上升高。Tet能抑制高K+,二氢吡啶类钙激动剂及兴奋性神经递质导致的胎鼠大脑[Ca2+]i含量增加,提示Tet对神经细胞损伤可能有一定保护作用。Cytosolic free Ca2+─[Ca2+]i was measured in dissociated cerebral cells isolatedfrom fetal rats using the fluorescent indicater Fura-2.Increases in[Ca2+]i occurred rapidly followingexposure of the cells to 50 mmol·L-1 KCl,10-7 mol·L-1 Bay K 8644 and 200 umol·L-1 glu-tamate(Glu ).[ Ca2+]i elevation produced by K+ -depolarization was blocked completely by pretreat-ment with tetrandrine(Tet)of various concentrations(10-9~ 10-7 mol·L-1,final).Tet showedsignificant inhibitory effect on[Ca2+]i increases stimufated by Glu in concentration-dependentmanner.With Tet 10-7 mol·L-1,Bay K 8644-induced increases in[Ca2+]i were reduced_markedly.These results indicate that Tet can block the increases in [Ca2+]i in fetal rat cerebral cellsinduced by Ca2+ agonists,suggesting that this drug may have a protective effect on cerebral cellinJury.
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