BACKGROUND: The protective effect of excitatory amino acid antagonists for CA3 hippocampal neuronal loss has been well documentated. From a clinical point of view, however, alternative therapies should also be explored because excitatory amino acid antagonists have relatively deleterious side effects. Administration of lecithinized superoxide dismutase (PC-SOD) has recently been demonstrated to reduce brain edema after traumatic brain injury (TBI) in the cerebral cortex. In this study, we investigated the effectiveness of PC-SOD on CA3 hippocampal cell loss by examining hematoxylin and eosin-stained sections. METHODS: Rats were divided at random into three groups. The first group received 1 mL of saline (contusion + saline group, n = 5). Rats of the second group were treated with 3000 IU/kg of PC-SOD (contusion + SOD 1 group, n = 5), while the third group received 5000 IU/kg of PC-SOD (contusion + SOD 2 group, n = 5). All agents were administered intraperitoneally 1 minute after traumatic insult and every 24 hours until 2 or 3 days post-TBI. Animals were sacrificed 3 or 7 days after contusion injury. RESULTS: PC-SOD prevented CA3 neuronal loss 3 days after TBI, and increased the number of surviving CA3 neurons 7 days after TBI. CONCLUSION: Our findings suggest that PC-SOD may serve as a pharmacological agent in the treatment of neuronal loss after TBI.
BACKGROUND: The protective effect of excitatory amino acid antagonists for CA3 hippocampal neuronal loss has been well documentated. From a clinical point of view, however, alternative therapies should also be explored because excitatory amino acid antagonists have relatively deleterious side effects. Administration of lecithinized superoxide dismutase (PC-SOD) has recently been demonstrated to reduce brain edema after traumatic brain injury (TBI) in the cerebral cortex. In this study, we investigated the effectiveness of PC-SOD on CA3 hippocampal cell loss by examining hematoxylin and eosin-stained sections. METHODS:Rats were divided at random into three groups. The first group received 1 mL of saline (contusion + saline group, n = 5). Rats of the second group were treated with 3000 IU/kg of PC-SOD (contusion + SOD 1 group, n = 5), while the third group received 5000 IU/kg of PC-SOD (contusion + SOD 2 group, n = 5). All agents were administered intraperitoneally 1 minute after traumatic insult and every 24 hours until 2 or 3 days post-TBI. Animals were sacrificed 3 or 7 days after contusion injury. RESULTS: PC-SOD prevented CA3 neuronal loss 3 days after TBI, and increased the number of surviving CA3 neurons 7 days after TBI. CONCLUSION: Our findings suggest that PC-SOD may serve as a pharmacological agent in the treatment of neuronal loss after TBI.
Authors: F J F Broeyer; B E van Aken; J Suzuki; M J B Kemme; H C Schoemaker; A F Cohen; Y Mizushima; J Burggraaf Journal: Br J Clin Pharmacol Date: 2007-07-04 Impact factor: 4.335
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Authors: Ulrich-Wilhelm Thomale; Martin Griebenow; Stefan-Nikolaus Kroppenstedt; Andreas W Unterberg; John F Stover Journal: Intensive Care Med Date: 2005-10-26 Impact factor: 17.440
Authors: Mathew B Potts; Seong-Eun Koh; William D Whetstone; Breset A Walker; Tomoko Yoneyama; Catherine P Claus; Hovhannes M Manvelyan; Linda J Noble-Haeusslein Journal: NeuroRx Date: 2006-04