Kita T, Shimada K, Mastunari Y, Wagner G C, Kubo K, Nakashima T
Department of Pharmacology, Nara Medical University, Kashihara, Japan.
Neuropharmacology. 2000 Jan 28;39(3):399-406. doi: 10.1016/s0028-3908(99)00175-6.
The expression of cyclooxygenase-2 (COX-2) and striatal dopamine (DA) depletion in BALB/cAnNcrj (BALB/c) mice following a neurotoxic dose of methamphetamine (METH) was investigated. METH-treatment (4 mg/kg x 4, 2 h intervals, s.c.) induced a significant hyperthermia and a persistent depletion of striatal DA levels 72 h after the treatment. COX-2, a marker of the cytotoxic effect of inflammation and oxidative stress and thiobarbituric acid (TBA) were significantly induced in the striatum 72 h after the METH-treatment, but not in the hippocampus. These results suggest that COX-2 may participate in METH-induced neurotoxicity in striatum.
研究了给予神经毒性剂量的甲基苯丙胺（METH）后，BALB/cAnNcrj（BALB/c）小鼠中环氧合酶-2（COX-2）的表达及纹状体多巴胺（DA）耗竭情况。METH处理（4mg/kg×4次，间隔2小时，皮下注射）在处理后72小时诱导了显著的体温过高以及纹状体DA水平的持续耗竭。COX-2是炎症和氧化应激细胞毒性作用的标志物，在METH处理后72小时，纹状体中COX-2和硫代巴比妥酸（TBA）显著诱导，但海马中未出现。这些结果表明COX-2可能参与了METH诱导的纹状体神经毒性。
