Curcumin Attenuates Hypoxia-Induced Oxidative Neurotoxicity, Apoptosis, Calcium, and Zinc Ion Influxes in a Neuronal Cell Line: Involvement of TRPM2 Channel

Armağan, Hamit Hakan; Nazıroğlu, Mustafa

doi:10.1007/s12640-020-00314-w

Cited by 12 publications

(40 citation statements)

References 43 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Present literature data indicated that the existence of TSPO induces the upregulation of mitochondrial redox signaling and PARP-1 activation, resulting in upregulated values of intracellular [Ca 2+ ] c , causing to stimulation of the Ca 2+ -mediated NADPH oxidase, thereby upregulating fROS values [24,25]. The TRPM2 channel is stimulated by NADPH oxidaseinduced fROS and PARP-1 activation-induced ADPR generations [22,35,36], although the channel is inhibited in several cells by the inhibitors of NADPH oxidase (apocynin), PARP-1 (DPQ and PJ34) and stimulation of GSH [21,22,31,37]. Similarly, the regulator role of TSPO deletion on the NADPH oxidase and PARP-1 activation in mice microglia was reported [24,25].…”

Section: Discussionmentioning

confidence: 99%

“…The increases of apoptosis and cell death are induced by the excessive Ca 2+ accumulation into mitochondria [44]. Even though the role of excessive Ca 2+ influx-mediated programmed cell death in neuronal injury has been discussed in several studies [21,23,30,31], TRPM2 activation-mediated apoptosis has not been explained in the ARPE19 yet. In the presence of excessive Ca 2+ influx into cytosol of retinal pigment epithelium, the pore of mitochondrial permeability transition (mPTP) has been shown to open in response to the mitochondrial Ca 2+ overload and ATP depletion [45].…”

Section: Discussionmentioning

confidence: 99%

“…Stimulation group: The cells in the group were stimulated by extracellular H 2 O 2 (1 mM) for 5 min or intracellular ADPR [20,21,30,31].…”

Section: Experimental Designmentioning

confidence: 99%

See 2 more Smart Citations

Deletion of Mitochondrial Translocator Protein (TSPO) Gene Decreases Oxidative Retinal Pigment Epithelial Cell Death via Modulation of TRPM2 Channel

Özkaya

Shu

Nazıroğlu

2021

Biology

Self Cite

View full text Add to dashboard Cite

The current results indicated the possible protective actions of 18 kDa mitochondrial translocator protein (TSPO) deletion on TRPM2 stimulation, mitochondrial free ROS (Mito-fROS) and apoptotic harmful actions in the cells of adult retinal pigment epithelial19 (ARPE19). There was a direct relationship between TSPO and the disease of age-related macular degeneration. The nature of TSPO implicates upregulation of Mito-fROS and apoptosis via the activation of Ca2+ channels in ARPE19, although deletion of TSPO gene downregulates the activation. The decrease of oxidative cytotoxicity and apoptosis might induce in TSPO gene deleted cells by the inhibition of Mito-fROS and PARP-1 activation-induced TRPM2 cation channel activation. The ARPE19 cells were divided into two main groups as TSPO expressing (ARPE19) and non-expressing cells (ARPE19-KO). The levels of caspase -3 (Casp -3), caspase -9 (Casp -9), apoptosis, Mito-fROS, TRPM2 current and intracellular free Ca2+ were upregulated in the ARPE19 by the stimulations of H2O2 and ADP-ribose, although their levels were downregulated in the cells by the modulators of PARP-1 (DPQ and PJ34), TRPM2 (ACA and 2APB) and glutathione. However, the H2O2 and ADP-ribose-mediated increases were not observed in the ARPE19-KO. The expression levels of Bax, Casp -3, Casp -9 and PARP-1 were higher in the ARPE19 group as compared to the ARPE19-KO group. In summary, current results confirmed that TRPM2-mediated cell death and oxidative cytotoxicity in the ARPE19 cells were occurred by the presence of TSPO. The deletion of TSPO may be considered as a therapeutic way to TRPM2 activation-mediated retinal oxidative injury.

show abstract

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Deletion of Mitochondrial Translocator Protein (TSPO) Gene Decreases Oxidative Retinal Pigment Epithelial Cell Death via Modulation of TRPM2 Channel

Özkaya

Shu

Nazıroğlu

2021

Biology

Self Cite

View full text Add to dashboard Cite

show abstract

“…Many reviews discussed the use of curcumin to treat diseases of the central nervous system (CNS), including Parkinson's, Alzheimer's, Huntington's disease, and multiple sclerosis [3,[7][8][9][10]. In an in vitro experimental model of neurodegenerative disease, Armagan and Naziroglu [11] reported the neuroprotective action of curcumin by modulating oxidative stress. In addition, this polyphenol is capable to decrease neurotoxicity, which is proven by other models of neurological disorders in vitro [11][12][13][14][15] and in vivo studies [16,17].…”

Section: Introductionmentioning

confidence: 99%

“…In an in vitro experimental model of neurodegenerative disease, Armagan and Naziroglu [11] reported the neuroprotective action of curcumin by modulating oxidative stress. In addition, this polyphenol is capable to decrease neurotoxicity, which is proven by other models of neurological disorders in vitro [11][12][13][14][15] and in vivo studies [16,17].…”

Section: Introductionmentioning

confidence: 99%

Impact of Free Curcumin and Curcumin Nanocapsules on Viability and Oxidative Status of Neural Cell Lines

Bissacotti

Copetti

Gündel

et al. 2021

Preprint

View full text Add to dashboard Cite

Curcumin is an active polyphenol substance found in the highest concentrations in the roots of Curcuma longa. Its health benefits have led to recent increases in the consumption of curcumin. It has anti-inflammatory and antioxidant activities and is a potent neuroprotective against diseases of the brain. Nevertheless, its low bioavailability and its relative difficulty crossing the blood-brain barrier limit curcumin’s use for these purposes. Curcumin-loaded nanoparticles may be an effective treatment for several diseases although there is a paucity of studies reporting its safety in the central nervous system (CNS). Therefore, this study aimed to identify non-neurotoxic concentrations of free curcumin and two nanoformulations of curcumin. Cell lines BV-2 and SH-SY5Y, both originating from the CNS, were evaluated after 24, 48, and 72 h of treatment with free curcumin and nanocapsules We measured viability, proliferation and dsDNA levels. We measured levels of reactive oxygen species and nitric oxide as proxies for oxidative stress in culture supernatants. We found that free curcumin was toxic at 10 and 20 µM, principally at 72 h. Nanoformulations were more neurotoxic than the free form. Safe concentrations of free curcumin are between 1-5 µM, and these concentrations were lower for nanoformulations. We determined the ideal concentrations of free curcumin and nanocapsules serving as a basis for studies of injuries that affect the CNS.

show abstract

Interferon Gamma-Mediated Oxidative Stress Induces Apoptosis, Neuroinflammation, Zinc Ion Influx, and TRPM2 Channel Activation in Neuronal Cell Line: Modulator Role of Curcumin

et al. 2021

View full text Add to dashboard Cite

Curcumin Attenuates Hypoxia-Induced Oxidative Neurotoxicity, Apoptosis, Calcium, and Zinc Ion Influxes in a Neuronal Cell Line: Involvement of TRPM2 Channel

Cited by 12 publications

References 43 publications

Deletion of Mitochondrial Translocator Protein (TSPO) Gene Decreases Oxidative Retinal Pigment Epithelial Cell Death via Modulation of TRPM2 Channel

Deletion of Mitochondrial Translocator Protein (TSPO) Gene Decreases Oxidative Retinal Pigment Epithelial Cell Death via Modulation of TRPM2 Channel

Impact of Free Curcumin and Curcumin Nanocapsules on Viability and Oxidative Status of Neural Cell Lines

Interferon Gamma-Mediated Oxidative Stress Induces Apoptosis, Neuroinflammation, Zinc Ion Influx, and TRPM2 Channel Activation in Neuronal Cell Line: Modulator Role of Curcumin

Contact Info

Product

Resources

About