An optimized triphenyltetrazolium chloride method for identification of cerebral infarcts

Joshi, Chintamani Narasinh; Jain, Swatantra Kumar; Murthy, Puvvada Sri Ramachandra

doi:10.1016/j.brainresprot.2003.12.001

Cited by 148 publications

(90 citation statements)

References 14 publications

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“…Whole brains were extracted and chilled at Ϫ20°C for 10 min. Coronal brain sections were made and incubated in 2% 2,3,5-triphenyltetrazolium chloride (TTC) in saline solution for 30 min at 37°C (Joshi et al, 2004).…”

Section: Methodsmentioning

confidence: 99%

Inhibition of Caspase-Mediated Apoptosis by Peroxynitrite in Traumatic Brain Injury

Lau¹,

Arundine²,

Sun³

et al. 2006

J. Neurosci.

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In traumatic brain injury (TBI), neurons surviving the primary insult may succumb through poorly understood secondary mechanisms. In vitro, cortical neurons exposed to stretch injury exhibited enhanced vulnerability to NMDA, apoptotic-like DNA fragmentation, peroxynitrite (PN) formation, and cytoplasmic cytochrome c accumulation. Surprisingly, caspase-3 activity was undetectable by both immunoblotting and fluorogenic activity assays. Therefore, we hypothesized that PN directly inhibits caspases in these neurons. Consistent with this, stretch injury in cultured neurons elicited tyrosine nitration of procaspase-3, but not caspase-9 or Apaf-1, suggesting a direct interaction of PN with caspase-3. In an ex vivo system, PN inhibited the activity of caspase-3, and this inhibition was reversible with the addition of the sulfhydryl reducing agent dithiothreitol, indicating that PN inhibits caspases by cysteinyl oxidation. Moreover, in cultures, the PN donor 3-morpholinosydnonimine (SIN-1) blocked staurosporine-induced caspase-3 activation and its downstream effects including PARP-1 [poly-(ADP-ribose) polymerase-1] cleavage and phosphotidylserine inversion, suggesting that peroxynitrite can inhibit caspase-3-mediated apoptosis. To examine these mechanisms in vivo, rats were exposed to a lateral fluid percussion injury (FPI). FPI caused increased neuronal protein nitration that colocalized with TUNEL staining, indicating that PN was associated with neurodegeneration. Caspase-3 activity was inhibited in brain lysates harvested after FPI and was restored by adding dithiothreitol. Our data show that caspase-mediated apoptosis is inhibited in neurons subjected to stretch in vitro and to TBI in vivo, mostly because of cysteinyl oxidation of caspase-3 by PN. However, this is insufficient to prevent cell death, indicating that the TBI therapy may, at a minimum, require a combination of both anti-apoptotic and anti-oxidant strategies.

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Section: Methodsmentioning

confidence: 99%

Inhibition of Caspase-Mediated Apoptosis by Peroxynitrite in Traumatic Brain Injury

Lau¹,

Arundine²,

Sun³

et al. 2006

J. Neurosci.

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“…Infarct areas were first measured using image analyzer software (Image J, version 1.47). Then, the total infarct volume of each brain was calculated using the following formula [17]:…”

Section: Evaluating Cerebral Infarct Volumementioning

confidence: 99%

Neuroprotective effect of safranal, an active ingredient of Crocus sativus , in a rat model of transient cerebral ischemia

Sadeghnia¹,

Shaterzadeh²,

Forouzanfar³

et al. 2017

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“…The slices were stained by 0.5% 2,3,5-triphenyltetrazoilum chloride (TTC; Sigma) and dissolved in physiologic buffer solution for 30 minutes at 37°C in the dark. 21 The sections were washed twice with saline, fixed with 4% paraformaldehyde for 30 minutes at room temperature, and then registered for image analysis. Brain infarct size was measured in ImageJ software (version 1.0; US National Institutes of Health, Bethesda, MD, USA), and infarct areas were integrated for calculating infarct volume.…”

Section: Determining Infarct Volumementioning

confidence: 99%

CDK5 Knockdown Prevents Hippocampal Degeneration and Cognitive Dysfunction Produced by Cerebral Ischemia

Gutiérrez-Vargas

Múnera

Cardona‐Gómez

2015

J Cereb Blood Flow Metab

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Acute ischemic stroke is a cerebrovascular accident and it is the most common cause of physical disabilities around the globe. Patients may present with repeated ictuses, experiencing mental consequences, such as depression and cognitive disorders. Cyclindependent kinase 5 (CDK5) is a kinase that is involved in neurotransmission and plasticity, but its dysregulation contributes to cognitive disorders and dementia. Gene therapy targeting CDK5 was administered to the right hippocampus of ischemic rats during transient cerebral middle artery occlusion. Physiologic parameters (blood pressure, pH, pO 2 , and pCO 2 ) were measured. The CDK5 downregulation resulted in neurologic and motor improvement during the first week after ischemia. Cyclin-dependent kinase 5 RNA interference (RNAi) prevented dysfunctions in learning, memory, and reversal learning at 1 month after ischemia. These observations were supported by the prevention of neuronal loss, the reduction of microtubule-associated protein 2 (MAP2) immunoreactivity, and a decrease in astroglial and microglia hyperreactivities and tauopathy. Additionally, CDK5 silencing led to an increase in the expression of brain-derived neurotrophic factor (BDNF), its Tropomyosin Receptor kinase B (TRKB) receptor, and activation of cyclic AMP response element-binding protein (CREB) and extracellular signal-regulated kinase (ERK), which are important targets in neuronal plasticity. Together, our findings suggest that gene therapy based on CDK5 silencing prevents cerebral ischemia-induced neurodegeneration and motor and cognitive deficits.

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An optimized triphenyltetrazolium chloride method for identification of cerebral infarcts

Cited by 148 publications

References 14 publications

Inhibition of Caspase-Mediated Apoptosis by Peroxynitrite in Traumatic Brain Injury

Inhibition of Caspase-Mediated Apoptosis by Peroxynitrite in Traumatic Brain Injury

Neuroprotective effect of safranal, an active ingredient of Crocus sativus , in a rat model of transient cerebral ischemia

CDK5 Knockdown Prevents Hippocampal Degeneration and Cognitive Dysfunction Produced by Cerebral Ischemia

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