Alpha lipoic acid attenuates hypoxia-induced apoptosis, inflammation and mitochondrial oxidative stress via inhibition of TRPA1 channel in human glioblastoma cell line

Deveci, Hacı; Akyuva, Yener; Nur, Gökhan; Nazıroğlu, Mustafa

doi:10.1016/j.biopha.2018.12.077

Cited by 63 publications

(41 citation statements)

References 39 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Mitochondria act major actions in neuronal ATP metabolism, energy homeostasis, the oxidative stress and apoptosis (Joshi and Bakowska 2012;Keil et al 2011). Regulation of mitochondrial Ca 2+ uptake could counteract HPX-induced mitochondrial membrane depolarization suppression, stimulate recovery of mitochondrial homeostasis, reduce neuronal oxidative injury and apoptosis, and enhance tissue repair and regeneration in the DBTRG neuronal cells (Cheng et al 2017;Khan et al 2017;Deveci et al 2019). It was reported that LEV modulates mitochondrial biogenesis and attenuates mitochondrial dysfunction, apoptosis and cell death in the HPX-induced oxidative stress of H9C2 cardiomyocyte cells (Sun et al 2014).…”

Section: Discussionmentioning

confidence: 99%

Levetiracetam modulates hypoxia-induced inflammation and oxidative stress via inhibition of TRPV1 channel in the DBTRG glioblastoma cell line

Ertilav

2020

Journal of Cellular Neuroscience and Oxidative Stress

View full text Add to dashboard Cite

show abstract

Section: Discussionmentioning

confidence: 99%

Levetiracetam modulates hypoxia-induced inflammation and oxidative stress via inhibition of TRPV1 channel in the DBTRG glioblastoma cell line

Ertilav

2020

Journal of Cellular Neuroscience and Oxidative Stress

View full text Add to dashboard Cite

show abstract

“…Several physiological and pathophysiological functions in normal and cancer cells are arranged by the calcium ion (Ca 2+ ) signaling. Tumor cell proliferation, including glioblastoma cell proliferation is controlled by the cytosolic basal neuronal Ca 2+ changes (Amantini et al 2007;Nazıroğlu 2007;Deveci et al 2019). On the other hand, during apoptosis and death, brain and glioblastoma cells enhance intracellular Ca 2+ influx (Kanu et al 2009;Kumar et al 2014) and activate a pathway of factors such as reactive oxygen species (ROS) generation and inflammation that when produced in excess can lead to tumor cell death (Morrone et al 2016;Ataizi et al 2019).…”

Section: Research Articlementioning

confidence: 99%

Clostridium botulinum neurotoxin A inhibits DBTRG glioblastoma cell proliferation and TRPV1 channel signaling pathways

Akyuva¹

2020

Journal of Cellular Neuroscience and Oxidative Stress

Self Cite

View full text Add to dashboard Cite

Journal of Cellular Neuroscience and Oxidative Stress is an online journal that publishes original research articles, reviews and short reviews on the molecular basis of biophysical, physiological and pharmacological processes that regulate cellular function, and the control or alteration of these processes by the action of receptors, neurotransmitters, second messengers, cation, anions, drugs or disease. Areas of particular interest are four topics. They are; A-Ion Channels (Na +-K + Channels, Clchannels, Ca 2+ channels, ADP-Ribose and metabolism of NAD + , Patch-Clamp applications) B-Oxidative Stress (Antioxidant vitamins, antioxidant enzymes, metabolism of nitric oxide, oxidative stress, biophysics, biochemistry and physiology of free oxygen radicals) C-Interaction Between Oxidative Stress and Ion Channels in Neuroscience (Effects of the oxidative stress on the activation of the voltage sensitive cation channels, effect of ADP-Ribose and NAD + on activation of the cation channels which are sensitive to voltage, effect of the oxidative stress on activation of the TRP channels in neurodegenerative diseases such Parkinson's and Alzheimer's diseases) D-Gene and Oxidative Stress (Gene abnormalities. Interaction between gene and free radicals. Gene anomalies and iron. Role of radiation and cancer on gene polymorphism)

show abstract

“…Hence, TRPM2 channels serve as targets of therapeutic agents to limit tumor growth and tumor-induced Ca 2+ entry in cancer treatments [54]. Moreover, alpha lipoic acid has been shown to attenuate hypoxia-induced apoptosis, inflammation, and mitochondrial oxidative stress via inhibition of the TRPA1 channel in a human glioblastoma cell line [55].…”

Section: Introductionmentioning

confidence: 99%

Resveratrol Enhances Apoptotic and Oxidant Effects of Paclitaxel through TRPM2 Channel Activation in DBTRG Glioblastoma Cells

Öztürk

Günaydın

Yalçın

et al. 2019

Oxidative Medicine and Cellular Longevity

Self Cite

View full text Add to dashboard Cite

Numerous studies have reported a strong association between increased production of reactive oxygen species (ROS) and the pathobiology of several diseases, and cancer in particular. Therefore, manipulation of cellular oxidative stress levels represents an important therapeutic target. Recently, resveratrol (RESV), a naturally occurring phytochemical, has been shown to sensitize several cell lines to the anticancer effects of other chemotherapeutic agents, including paclitaxel (PAX). However, the molecular mechanisms of action of RESV through oxidative sensitive TRPM2 channel activation remain unclear. The aim of this study was to evaluate the effect of combination therapy of RESV and PAX on activation of TRPM2 in DBTRG glioblastoma cells. DBTRG cells were divided into four treatment groups: control, RESV (50 μM), PAX (50 μM), and PAX + RESV for 24 hours. Our data shows that markers for apoptosis, mitochondrial membrane depolarization and mitochondrial function, intracellular steady-state ROS levels, caspase 3 activity, TRPM2 current density, and Ca2+ florescence intensity were significantly increased in DBTRG cells following treatment with PAX and RESV, respectively, although cell viability was also decreased by these treatments. These biochemical markers were further increased to favor the anticancer effects of PAX in DBTRG cells in combination with RESV. The PAX and RESV-mediated increase in current density and Ca2+ florescence intensity was decreased with a TRPM2 blocker. This suggests that for this combination therapy to have a substantial effect on apoptosis and cell viability, the TRPM2 channel must be stimulated.

show abstract

Alpha lipoic acid attenuates hypoxia-induced apoptosis, inflammation and mitochondrial oxidative stress via inhibition of TRPA1 channel in human glioblastoma cell line

Cited by 63 publications

References 39 publications

Levetiracetam modulates hypoxia-induced inflammation and oxidative stress via inhibition of TRPV1 channel in the DBTRG glioblastoma cell line

Levetiracetam modulates hypoxia-induced inflammation and oxidative stress via inhibition of TRPV1 channel in the DBTRG glioblastoma cell line

Clostridium botulinum neurotoxin A inhibits DBTRG glioblastoma cell proliferation and TRPV1 channel signaling pathways

Resveratrol Enhances Apoptotic and Oxidant Effects of Paclitaxel through TRPM2 Channel Activation in DBTRG Glioblastoma Cells

Contact Info

Product

Resources

About