Neuroprotective effects of the antifungal drug clotrimazole

Isaev, N. K.; Stelmashook, E. V.; Dirnagl, Ulrich; Andreeva, N. A.; Manuhova, L; Vorobjev, Vladimir S.; Шаронова, И. Н.; Skrebitsky, V. G.; Victorov, Ilya V.; Katchanov, Juri; Weih, Markus; Zorov, Dmitry B.

doi:10.1016/s0306-4522(02)00164-1

Cited by 42 publications

(26 citation statements)

References 15 publications

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“…# Differences statistically significant vs. 5 µM TBBPA (one-way ANOVA followed by Dunnett's test, p < 0.05) When examining the putative mechanism of TBBPA and OGD synergy we considered calcium imbalance, mitochondrial disfunction and oxidative stress. According to literature data, these processes might be common to both of toxic factors studied here [9,14,22,23,25,27,28,32]. Therefore, using standard methods we measured…”

Section: Ros Mediate Tbbpa and Ogd Synergy In Cgc Culturesmentioning

confidence: 97%

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Synergistic neurotoxicity of oxygen-glucose deprivation and tetrabromobisphenol A in vitro: role of oxidative stress

Ziemińska

Stafiej

Toczyłowska

et al. 2012

Pharmacological Reports

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Abstract:Background: Tetrabromobisphenol A (TBBPA) is a toxic brominated flame retardant. Previous studies have demonstrated that exposure of primary cultures of rat cerebellar granule cells (CGC) to ³ 10 µM TBBPA induces toxicity and excitotoxicity, and the underlying mechanism may involve calcium imbalance and oxidative stress. Here we examined whether the application of TBBPA at subtoxic concentrations may exacerbate acute damage of CGC challenged with oxygen-glucose deprivation (OGD), and evaluated with fluorescent indicators the involvement of calcium imbalance, mitochondrial depolarization and oxidative stress. Methods: Survival of CGC was assessed 24 h after OGD/TBBPA using fluorescent dyes. An OGD challenge lasting for 45, 60 or 75 min induced a duration-dependent injury to the neurons. Results: Application of 2.5, 5 or 7.5 µM TBBPA for 45 min to normoxic and glucose-containing incubation medium did not reduce the viability of cultured CGC, but this compound exacerbated the toxic effects of OGD in a concentration-dependent way. Moreover, TBBPA had a slight effect on calcium homeostasis and mitochondrial membrane potential, but significantly activated the production of reactive oxygen species in CGC. The application of H 2 O 2 at 5, 10 and 25 µM mimicked the effects of TBBPA on OGD toxicity, while 0.1 mM ascorbic acid or 1 mM glutathione ameliorated this toxicity. Conclusion: These results suggest the involvement of oxidative stress in the synergistic neurotoxic effects of TBBPA and OGD.

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Section: Ros Mediate Tbbpa and Ogd Synergy In Cgc Culturesmentioning

confidence: 97%

“…In our present experiments, 45, 60 or 75 min OGD resulted in a significant reduction in the number of live neurons, which was dependent on the duration of these conditions. Previous studies in which CGC have been challenged with OGD used similar durations of this treatment to induce significant neuronal degeneration [14,16,32].…”

mentioning

confidence: 99%

Synergistic neurotoxicity of oxygen-glucose deprivation and tetrabromobisphenol A in vitro: role of oxidative stress

Ziemińska

Stafiej

Toczyłowska

et al. 2012

Pharmacological Reports

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“…Glutamate-induced increases in [Ca 2+ ]i involved the influx of Ca 2+ from the extracellular milieu. The inability of neurons to reverse the increase in [Ca 2+ ] and to maintain a normal [Ca 2+ ]i was considered a key mechanism of neuronal death after toxic glutamate treatment (Isaev et al 2002).…”

Section: Influence Of Pilocarpine On Calcium Homeostasis In Glutamatementioning

confidence: 99%

Neuroprotection of Muscarinic Receptor Agonist Pilocarpine Against Glutamate-induced Apoptosis in Retinal Neurons

Zhou

Zhu

et al. 2008

Cell Mol Neurobiol

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Neuroprotection offers potential as an alternative therapy for glaucoma. Pilocarpine, as a typical muscarinic receptor agonist, remains among the major intraocular pressure lowering drugs for the conventional treatment of glaucoma. However, whether pilocarpine also possesses neuroprotection against glutamate cytotoxicity in retinal neurons is still unknown. In rat primary retinal cultures, identification of neuron, cell viability, apoptosis, intracellular Ca(2+) concentration, mitochondrial membrane potential, gene expression were studied by immunofluorescence, MTT, High Content Scanning, confocal microscopy, reverse-transcription PCR, and western blot analysis, respectively. Pretreatment of pilocarpine could prevent glutamate-induced neuron death, which was blocked by the non-selective antagonist atropine and the M1-selective muscarinic receptor antagonist pirenzepine. The antiapoptotic effect of pilocarpine was associated with maintaining calcium homeostasis, recovering mitochondrial membrane potential, and regulating the expression of Bcl-2 and Caspase-3. These studies demonstrated that pilocarpine had effective protection against glutamate-induced neuronal apoptosis through M1 muscarinic receptor. The results may provide an insight into the new mechanism of glaucoma therapy that pilocarpine may potentially act as a retinal neuroprotectant.

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“…Primary hippocampal cultures were prepared from 2-day-old Sprague-Dawley rats as described by Isaev et al (2002) with modifications. Briefly, the tissue was digested with 0.25% trypsin in phosphate-buffered saline (PBS) for 20 min at 37 • C followed by mechanical dissociation.…”

Section: Primary Hippocampal Cell Culturementioning

confidence: 99%

Potential involvement of calcium and nitric oxide in protective effects of puerarin on oxygen–glucose deprivation in cultured hippocampal neurons

Zheng

2007

Journal of Ethnopharmacology

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Neuroprotective effects of the antifungal drug clotrimazole

Cited by 42 publications

References 15 publications

Synergistic neurotoxicity of oxygen-glucose deprivation and tetrabromobisphenol A in vitro: role of oxidative stress

Synergistic neurotoxicity of oxygen-glucose deprivation and tetrabromobisphenol A in vitro: role of oxidative stress

Neuroprotection of Muscarinic Receptor Agonist Pilocarpine Against Glutamate-induced Apoptosis in Retinal Neurons

Potential involvement of calcium and nitric oxide in protective effects of puerarin on oxygen–glucose deprivation in cultured hippocampal neurons

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