Liu T H, Beckman J S, Freeman B A, Hogan E L, Hsu C Y
Department of Neurology, Medical University of South Carolina, Charleston 29425-2232.
Am J Physiol. 1989 Feb;256(2 Pt 2):H589-93. doi: 10.1152/ajpheart.1989.256.2.H589.
Superoxide dismutase and catalase enzymatically scavenge superoxide and hydrogen peroxide, respectively. Conjugation of polyethylene glycol to superoxide dismutase (PEG-SOD) or catalase (PEG-CAT) prolongs the circulatory half-life of the native enzymes and enhances their intracellular access. We studied the protective effect of these free radical scavengers on ischemic brain injury using a rat model of focal cerebral ischemia, which is suitable for therapeutic trials. Intravenous administration of PEG-SOD (10,000 U/kg) and PEG-CAT (10,000 U/kg) before ischemia reduced the infarct volume (treatment, 139 +/- 9 mm3, means +/- SE, N = 38; placebo, 182 +/- 8 mm3, n = 37, P less than 0.002). This finding supports the concept that superoxide and hydrogen peroxide contribute to brain injury following focal cerebral ischemia.
超氧化物歧化酶和过氧化氢酶分别通过酶促作用清除超氧化物和过氧化氢。将聚乙二醇与超氧化物歧化酶(PEG-SOD)或过氧化氢酶(PEG-CAT)结合,可延长天然酶的循环半衰期并增强其细胞内摄取。我们使用适合治疗试验的局灶性脑缺血大鼠模型,研究了这些自由基清除剂对缺血性脑损伤的保护作用。缺血前静脉注射PEG-SOD(10,000 U/kg)和PEG-CAT(10,000 U/kg)可减少梗死体积(治疗组,139±9 mm³,均值±标准误,N = 38;安慰剂组,182±8 mm³,n = 37,P<0.002)。这一发现支持了超氧化物和过氧化氢在局灶性脑缺血后导致脑损伤的观点。