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The neuroprotective effects of AMN082 on neuronal apoptosis in rats after traumatic brain injury

Authors
  • Lu, Chung-Che1
  • Nyam, Tee-Tau Eric1
  • Kuo, Jinn-Rung1, 2
  • Lee, Yao-Lin1
  • Chio, Chung-Ching1
  • Wang, Che-Chuan1, 2, 3
  • 1 Chi-Mei Medical Center, 901 Chung Hwa Road, Yung Kang City, Tainan, Taiwan , Tainan (Taiwan)
  • 2 Chi-Mei Medical Center, Tainan, Taiwan , Tainan (Taiwan)
  • 3 Southern Taiwan University of Science and Technology, Tainan, Taiwan , Tainan (Taiwan)
Type
Published Article
Journal
BMC Neuroscience
Publisher
Springer (Biomed Central Ltd.)
Publication Date
Jun 25, 2021
Volume
22
Issue
1
Identifiers
DOI: 10.1186/s12868-021-00649-w
Source
Springer Nature
Keywords
Disciplines
  • Research
License
Green

Abstract

BackgroundThe aim of this study was to investigate whether AMN082 exerts its neuroprotective effect by attenuating glutamate receptor-associated neuronal apoptosis and improving functional outcomes after traumatic brain injury (TBI).MethodsAnesthetized male Sprague–Dawley rats were divided into the sham-operated, TBI + vehicle, and TBI + AMN082 groups. AMN082 (10 mg/kg) was intraperitoneally injected 0, 24, or 48 h after TBI. In the 120 min after TBI, heart rate, mean arterial pressure, intracranial pressure (ICP), and cerebral perfusion pressure (CPP) were continuously measured. Motor function, the infarct volume, neuronal nitrosative stress-associated apoptosis, and N-methyl-d-aspartate receptor 2A (NR2A) and NR2B expression in the pericontusional cortex were measured on the 3rd day after TBI.ResultsThe results showed that the AMN082-treated group had a lower ICP and higher CPP after TBI. TBI-induced motor deficits, the increase in infarct volume, neuronal apoptosis, and 3-nitrotyrosine and inducible nitric oxide synthase expression in the pericontusional cortex were significantly improved by AMN082 therapy. Simultaneously, AMN082 increased NR2A and NR2B expression in neuronal cells.ConclusionsWe concluded that intraperitoneal injection of AMN082 for 3 days may ameliorate TBI by attenuating glutamate receptor-associated nitrosative stress and neuronal apoptosis in the pericontusional cortex. We suggest that AMN082 administration in the acute stage may be a promising strategy for TBI.

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