The effect of N-acetylcysteine on posttraumatic changes after controlled cortical impact in rats

Thomale, Ulrich‐Wilhelm; Griebenow, Martin; Kroppenstedt, Stefan; Unterberg, Andreas; Stover, John

doi:10.1007/s00134-005-2845-4

Cited by 35 publications

(34 citation statements)

References 38 publications

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“…These results correlate well with the literatures (Hicdonmez et al 2006;Rink et al 1995;Thomale et al 2006;Shapira et al 1988). In our study, the most consistent findings in histological sections of neuron regions amongst the TBI group involved severe degenerative changes, shrunken cytoplasma and extensively dark picnotic nuclei.…”

Section: Discussionsupporting

confidence: 93%

Neuroprotective effects of Caffeic acid phenethyl ester on experimental traumatic brain injury in rats

et al. 2011

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The aim of this study was to evaluate the therapeutic efficacy of caffeic acid phenethyl ester (CAPE) with an experimental traumatic brain injury (TBI) model in rats. Twenty-four adult male Sprague-Dawley rats were randomly divided into three groups of 8 rats each: control, TBI, and TBI + CAPE treatment. In TBI and TBI + CAPE treatment groups, a cranial impact was delivered to the skull from a height of 7 cm at a point just in front of the coronal suture and over the right hemisphere. Rats were sacrificed at 4 h after the onset of injury. Brain tissues were removed for biochemical and histopathological investigation. To date, no biochemical and histopathological changes of neurodegeneration in the frontal cortex after TBI in rats by CAPE treatment have been reported. The TBI significantly increased tissue malondialdehyde (MDA) levels, and significantly decreased tissue superoxide dismutase (SOD) and glutathione peroxidase (GPx) activities, but not tissue catalase (CAT) activity, when compared with controls. The administration of a single dose of CAPE (10 μmol/kg) 15 min after the trauma has shown protective effect via decreasing significantly the elevated MDA levels and also significantly increasing the reduced antioxidant enzyme (SOD and GPx) activities, except CAT activity. In the TBI group, severe degenerative changes, shrunken cytoplasma and extensively dark picnotic nuclei in neurons, as well as vacuolization indicating tissue edema formation. The morphology of neurons in the CAPE treatment group was well protected. The number of neurons in the trauma alone group was significantly less than that of both the control and TBI +CAPE treatment groups. The caspase 3 immunopositivity was increased in degenerating neurons of the traumatic brain tissue. Treatment of CAPE markedly reduced the immunoreactivity of degenerating neurons. TBI caused severe degenerative changes, shrunken cytoplasma, severely dilated cisternae of endoplasmic reticulum, markedly swollen mitochondria with degenerated cristae and nuclear membrane breakdown with chromatin disorganization in neurons of the frontal cortex. In conclusion, the CAPE treatment might be beneficial in preventing trauma-induced oxidative brain tissue damage, thus showing potential for clinical implications. We believe that further preclinical research into the utility of CAPE may indicate its usefulness as a potential treatment on neurodegeneration after TBI in rats.

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Section: Discussionsupporting

confidence: 93%

Neuroprotective effects of Caffeic acid phenethyl ester on experimental traumatic brain injury in rats

et al. 2011

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“…In that study, no significant positive effect on posttraumatic perfusion, brain edema formation, or contusion volume after brain injury was observed at 24 h with the NAC (163 mg/kg) having been administered immediately as well as at 2 and 4 h after the trauma. However, they concluded that the tendency of a statistically non-significant diminished contusion volume after NAC treatment demonstrated the need for further investigation into the protective effects of neuronal survival on the cellular level [47]. Our results, however, do support the suggestion of Thomale et al in terms of neuronal survival.…”

Section: Discussioncontrasting

confidence: 58%

“…Thomale et al, however, observed no effect of NAC treatment on posttraumatic edema formation [47]. In a previous experimental study, Unterberg et al reported that the development of brain edema was of a cytogenic and vasogenic nature after the controlled cortical injury, while cytogenic edema formation predominated [61].…”

Section: Discussionmentioning

confidence: 97%

“…The secondary injury at the subcellular level that follows the primary impact causes the death of additional tissue at the peripheral zone of the initial damage and is considered the main target of medical treatment. One important defense mechanism against oxidative stress involves the tripeptide glutathione [47]. Moreover, antioxidant enzyme activities have been found to be diminished under highly elevated oxidative stress conditions because of molecular damage.…”

Section: Discussionmentioning

confidence: 99%

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Neuroprotective Effects of N-acetylcysteine on Experimental Closed Head Trauma in Rats

et al. 2006

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N-acetylcysteine (NAC) is a precursor of glutathione, a potent antioxidant, and a free radical scavenger. The beneficial effect of NAC on nervous system ischemia and ischemia/reperfusion models has been well documented. However, the effect of NAC on nervous system trauma remains less understood. Therefore, we aimed to investigate the therapeutic efficacy of NAC with an experimental closed head trauma model in rats. Thirty-six adult male Sprague-Dawley rats were randomly divided into three groups of 12 rats each: Group I (control), Group II (trauma-alone), and Group III (trauma+NAC treatment). In Groups II and III, a cranial impact was delivered to the skull from a height of 7 cm at a point just in front of the coronal suture and over the right hemisphere. Rats were sacrificed at 2 h (Subgroups I-A, II-A, and III-A) and 12 h (Subgroups I-B, II-B, and III-B) after the onset of injury. Brain tissues were removed for biochemical and histopathological investigation. The closed head trauma significantly increased tissue malondialdehyde (MDA) levels (P < 0.05), and significantly decreased tissue superoxide dismutase (SOD) and glutathione peroxidase (GPx) activities (P < 0.05), but not tissue catalase (CAT) activity, when compared with controls. The administration of a single dose of NAC (150 mg/kg) 15 min after the trauma has shown protective effect via decreasing significantly the elevated MDA levels (P < 0.05) and also significantly (P < 0.05) increasing the reduced antioxidant enzyme (SOD and GPx) activities, except CAT activity. In the trauma-alone group, the neurons became extensively dark and degenerated into picnotic nuclei. The morphology of neurons in the NAC treatment group was well protected. The number of neurons in the trauma-alone group was significantly less than that of both the control and trauma+NAC treatment groups. In conclusion, the NAC treatment might be beneficial in preventing trauma-induced oxidative brain tissue damage, thus showing potential for clinical implications.

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“…27 However, in a study on rats with moderate left focal cortical contusion trauma, Thomale et al found that 163 mg/kg of NAC applied intraperitoneally 2-4 h after the brain injury was ineffective against post-traumatic perfusion, brain edema or contusion volume. 28 Cuzzocrea et al investigated the effect of NAC on brain ischemic injury in gerbils. Ischemia-reperfusion injury was induced in Mongolian gerbils by a single bilateral occlusion of the common carotid arteries, and NAC (20 mg/kg) was given intraperitoneally 30 min before and 1 h, 2 h, and 6 h after reperfusion.…”

Section: Discussionmentioning

confidence: 99%

The neuroprotective effect of N-acetylcysteine in spinal cord-injured rats

Olakowska¹,

Marcol²,

Właszczuk³

et al. 2017

Adv Clin Exp Med

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The effect of N-acetylcysteine on posttraumatic changes after controlled cortical impact in rats

Abstract: Despite previously reported neuroprotective abilities of NAC, no positive effect on posttraumatic perfusion, brain edema formation, or contusion volume after focal brain injury was observed in this study.

Cited by 35 publications

References 38 publications

Neuroprotective effects of Caffeic acid phenethyl ester on experimental traumatic brain injury in rats

Neuroprotective effects of Caffeic acid phenethyl ester on experimental traumatic brain injury in rats

Neuroprotective Effects of N-acetylcysteine on Experimental Closed Head Trauma in Rats

The neuroprotective effect of N-acetylcysteine in spinal cord-injured rats

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