Neuroprotective effects of Scrophularia buergeriana extract against glutamate-induced toxicity in SH-SY5Y cells

Lee, Hae Jin; Spandidos, Demetrios Α.; Tsatsakis, Aristidis; Margină, Denisa; Izotov, Boris N.; Yang, Seung Hwan

doi:10.3892/ijmm.2019.4139

Cited by 33 publications

(56 citation statements)

References 44 publications

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“…It was reported that glutamate at 1-50 mM concentration affected H 2 O 2 synthesis by brain mitochondria and this effect was associated with complex II, a source of superoxide anion formation in mitochondria and was dependent on the mitochondrial potential [31]. We found a non-significant increase in SOD activity which was not consistent with other studies that had reported a decrease with glutamate [18,32]. ROS is converted to less reactive hydrogen peroxide by SOD through the use of copper/zinc or manganese and could play a protective role in neurodegeneration and had been thought to be activated firstly for defense systems against oxidative stress, in neurodegeneration [33].…”

Section: Discussioncontrasting

confidence: 89%

The neuroprotective effect of lamotrigine against glutamate excitotoxicity in SH-SY5Y human neuroblastoma cells

Oğuz

Acet

Hodzic

et al. 2020

Marmara Medical Journal

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Objective: Glutamate-induced excitotoxicity has a role in the pathophysiology of neurodegenerative disorders. Lamotrigine, an antiepileptic drug, also used to treat bipolar disorders, may be protective against excitotoxic insult. The aim of the study was to investigate the neuroprotective effect of lamotrigine against the glutamate excitotoxicity in SH-SY5Y cell line. Materials and Methods: SH-SY5Y human neuroblastoma cells were pre-treated with lamotrigine (50-100-150 µM) prior to exposure to 15 mM glutamate. The 3-(4,5-dimethythiazol-2-yl)-2,5-diphenyl tetrazolium bromide (MTT) assay was performed to determine cell viability. The anti-oxidant effect of lamotrigine and the role of inflammatory parameters were determined by measuring superoxide dismutase (SOD), hydrogen peroxide (H 2 O 2), IL-1β, IL-6 and TNF-α. Results: Intracellular calcium levels and lactate dehydrogenase (LDH) activity increased in glutamate exposed cells. Pre-treatment of cells with MK-801 showed no protective features against glutamate excitotoxicity. Treatment with 100 µM lamotrigine was effective in increasing the viability of glutamate exposed cells and in reducing H 2 O 2 increase in these cells. The SOD activity increased by lamotrigine treated cells exposed to glutamate. IL-1β, IL-6 and TNF-α levels increased after induction with glutamate and attenuated by lamotrigine. Conclusion: Overall, our results confirmed the critical role of inflammation and oxidative stress in glutamate-induced excitotoxicity and lamotrigine may exert a protective effect.

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Section: Discussioncontrasting

confidence: 89%

The neuroprotective effect of lamotrigine against glutamate excitotoxicity in SH-SY5Y human neuroblastoma cells

Oğuz

Acet

Hodzic

et al. 2020

Marmara Medical Journal

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“…In the pathological condition, extensive DNA damage in cells results in PARP1 cleavage (inactive), preventing DNA repair and thereby leading to cell apoptosis or necrosis (Swindall et al, 2013 ; Morales et al, 2014 ). Abnormal PARP1 cleavage has been implicated in many diseases, such as the neurodegenerative diseases including PD (Lee et al, 2013 , 2019 ). Our studies not only provide novel insight into the biological roles of TMEM230 in the PARP1-linked pathway but also provide a TMEM230-induced cell death mechanism underlying PD-linked pathogenesis.…”

Section: Introductionmentioning

confidence: 99%

Transmembrane Protein 230 Mediates a Poly(ADP-ribose) Polymerase-1-Linked Apoptosis

Wang

Zhang

et al. 2020

Front. Aging Neurosci.

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Mutations in transmembrane protein 230 (TMEM230) gene are suggested to be associated with the autosomal dominant Parkinson's disease (PD) with typical movement disorders and Lewy body pathology. However, the normal functions and the pathological roles of TMEM230 are not clear. In this study, we used TMEM230 isoform II constructs including wild-type (WT) and four reported PD-linked mutation constructs (Y92C, R141L, 184Wext * 5, and 184PGext * 5). Ectopic expression of WT and PD-linked mutant TMEM230 variants in cultured cells dramatically induced apoptotic cell death compared with that of vector control cells. Mutant TMEM230 caused cell toxicity at an increased severity than WT TMEM230. Moreover, expression of TMEM230 increased mitochondrial reactive oxygen species (ROS) levels, decreased cellular ATP, activated caspase 3/7, and increased poly(ADP-ribose) polymerase-1 (PARP1) cleavage. Treatment with N-acetylcysteine (NAC; an ROS scavenger) or Z-VAD-FMK (a caspase inhibitor) significantly attenuated TMEM230-induced apoptosis in both cultured cells and primary neurons. Our results indicated that TMEM230 mediated a PARP1-linked apoptotic cell death pathway. These findings not only provide the novel insight into the biological roles of TMEM230 in the PARP1-linked pathway but also provide a TMEM230-induced cell death mechanism underlying PD pathogenesis.

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“…Hence, final stages of cell death in the two cell lines may differ. A contributory role of caspase-3 activity has been observed in many studies in the Glu-induced model of cell death of SH-SY5Y cells [ 62 , 77 , 78 , 79 ]. In this assay, neuron-like SH-SY5Y cells were treated here with 160 mM Glu, which leads to elevation of caspase-3/7 activity.…”

Section: Resultsmentioning

confidence: 99%

Cytokinin Plant Hormones Have Neuroprotective Activity in In Vitro Models of Parkinson’s Disease

et al. 2021

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Cytokinins are adenine-based phytohormones that regulate key processes in plants, such as cell division and differentiation, root and shoot growth, apical dominance, branching, and seed germination. In preliminary studies, they have also shown protective activities against human neurodegenerative diseases. To extend knowledge of the protection (protective activity) they offer, we investigated activities of natural cytokinins against salsolinol (SAL)-induced toxicity (a Parkinson’s disease model) and glutamate (Glu)-induced death of neuron-like dopaminergic SH-SY5Y cells. We found that kinetin-3-glucoside, cis-zeatin riboside, and N6-isopentenyladenosine were active in the SAL-induced PD model. In addition, trans-, cis-zeatin, and kinetin along with the iron chelator deferoxamine (DFO) and the necroptosis inhibitor necrostatin 1 (NEC-1) significantly reduced cell death rates in the Glu-induced model. Lactate dehydrogenase assays revealed that the cytokinins provided lower neuroprotective activity than DFO and NEC-1. Moreover, they reduced apoptotic caspase-3/7 activities less strongly than DFO. However, the cytokinins had very similar effects to DFO and NEC-1 on superoxide radical production. Overall, they showed protective activity in the SAL-induced model of parkinsonian neuronal cell death and Glu-induced model of oxidative damage mainly by reduction of oxidative stress.

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Neuroprotective effects of Scrophularia buergeriana extract against glutamate-induced toxicity in SH-SY5Y cells

Cited by 33 publications

References 44 publications

The neuroprotective effect of lamotrigine against glutamate excitotoxicity in SH-SY5Y human neuroblastoma cells

The neuroprotective effect of lamotrigine against glutamate excitotoxicity in SH-SY5Y human neuroblastoma cells

Transmembrane Protein 230 Mediates a Poly(ADP-ribose) Polymerase-1-Linked Apoptosis

Cytokinin Plant Hormones Have Neuroprotective Activity in In Vitro Models of Parkinson’s Disease

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