Erucic acid increases the potency of cisplatin-induced colorectal cancer cell death and oxidative stress by upregulating the TRPM2 channel.

Erucic acid (ErA) is a source of omega-9 monounsaturated fatty acids. ErA exhibited antitumor effects by causing apoptosis and oxidative stress in tumor cells, with the exception of the HT-29 human colorectal cancer cell line. The apoptotic and Ca signaling pathways in tumor cells are triggered when mitochondrial Ca and Zn accumulation produce reactive free oxygen species (ROS), which in turn activate TRPM2.

Examination of experienced coaches and physical education teachers' teaching methods and their perceptions regarding these methods-2023.

Introduction: It is widely acknowledged that coaches and physical education teachers play an important role in supporting holistic development in children and ensuring optimal performance in the training processes carried out to acquire fundamental movements and sport-specific basic skills. However, there is a need for further information on how both groups utilize and value different teaching methods during the training. The present study aims to examine the perceptions of coaches and physical education teachers regarding the use and value of teaching methods.

Synergic actions of botulinum neurotoxin A and oxaliplatin on colorectal tumour cell death through the upregulation of TRPM2 channel-mediated oxidative stress.

Botulinum neurotoxin A (BoNT) is being shown to have anticancer action as a potential adjuvant treatment. The transient receptor potential (TRP) melastatin 2 (TRPM2) stimulator action of BoNT was reported in glioblastoma cells, but not in colorectal cancer (HT29) cells. By activating TRPM2, we evaluated the impacts of BoNT and oxaliplatin (OXA) incubations on oxidant and apoptotic values within the HT29 cells.

Alpha-lipoic acid modulates the diabetes mellitus-mediated neuropathic pain via inhibition of the TRPV1 channel, apoptosis, and oxidative stress in rats.

Diabetes mellitus (DM) is a chronic syndrome involving neuropathic pain. Increased oxidative stress in DM is assumed to increase free reactive oxygen radicals (ROS) and causes diabetic damage. The sciatic nerve (ScN) and dorsal root ganglion (DRG) both contain high levels of the TRPV1 channel, which is triggered by capsaicin and ROSs and results in increased Ca entry into the neurons.

Curcumin attenuates hydroxychloroquine-mediated apoptosis and oxidative stress via the inhibition of TRPM2 channel signalling pathways in a retinal pigment epithelium cell line.

Purpose: Hydroxychloroquine (HCQ) is used in the treatment of several diseases, such as malaria, Sjögren's disease, Covid-19, and rheumatoid arthritis. However, HCQ induces retinal pigment epithelium death via the excessive increase of cytosolic (cROS) and mitochondrial (mROS) free oxygen radical production. The transient receptor potential melastatin 2 (TRPM2) cation channel is stimulated by ADP-ribose (ADPR), cROS, and mROS, although it is inhibited by curcumin (CRC).

Low molecular weight heparin treatment reduced apoptosis and oxidative cytotoxicity in the thrombocytes of patients with recurrent pregnancy loss and thrombophilia: Involvements of TRPM2 and TRPV1 channels.

Aim: Recurrent pregnancy loss (RPL) is known to be associated with increased thrombophilia and oxidative toxicity. However, the mechanism of thrombophilia apoptosis and oxidative toxicity is still unclear. In addition, the treatment of heparin induced regulator roles on intracellular free Ca ([Ca ] ) and cytosolic reactive oxygen species (cytROS) concentrations in several diseases.

NMDA Receptor Activation Stimulates Hypoxia-Induced TRPM2 Channel Activation, Mitochondrial Oxidative Stress, and Apoptosis in Neuronal Cell Line: Modular Role of Memantine.

TRPM2 channel is activated by the increase of hypoxia (HYP)-mediated excessive mitochondrial (mROS) and cytosolic (cROS) free reactive oxygen species generation and intracellular free Ca ([Ca]) influx. The stimulations of the N-methyl-d-aspartate(NMDA) receptor and TRPM2 channel induce mROS and apoptosis in the neurons, although their inhibitions via the treatments of memantine (MEM) and MK-801 decrease mROS and apoptosis. However, the molecular mechanisms underlying MEM treatment and NMDA inhibition' neuroprotection via TRPM2 inhibition in the HYP remain elusive.

Involvement of TRPM7 Channel on the Induction of Diabetic Neuropathic Pain in Mice: Protective Role of Selenium and Curcumin.

Excessive levels of the mitochondrial reactive oxygen radical (mitSOX) and Ca influx were found to cause neuropathic pain in patients with diabetes mellitus (DM). Naltriben (NLT) and mitSOX activate the transient receptor (TRP) melastatin 7 (TRPM7) channel, but antioxidants and carvacrol inhibit it. Selenium (Se) and curcumin (CRC) have been thoroughly studied for their modulator effects on streptozotocin (STZ)-induced neuropathic pain, apoptosis, and oxidative stress through the blockage of TRP channels in dorsal root ganglion (DRG) neurons.

Transient receptor potential channel stimulation induced oxidative stress and apoptosis in the colon of mice with colitis-associated colon cancer: modulator role of Sambucus ebulus L.

Background: Increased Ca entry causes an increase in tumor cell proliferation, apoptosis, cytosolic reactive free oxygen species (cyROS), and mitochondrial ROS (miROS) in tumor cells. The cyROS and miROS stimulate the cation channels, including the TRPA1, TRPM2, and TRPV1. Sambucus ebulus L (SEB) (Dwarf Elder) induced both antioxidant and anticancer effects in the human hepatocarcinoma and human colon carcinoma cancer cell lines.

Honey bee venom melittin increases the oxidant activity of cisplatin and kills human glioblastoma cells by stimulating the TRPM2 channel.

Melittin (MLT) treatment is believed to enhance tumor cell death, apoptotic, and oxidative cytotoxic effects of cisplatin (CSP) via the modulation of Ca channels in several cancer lines. The activation of TRPM2 mediated anticancer and CSP resistance actions via mitochondrial Ca and Zn accumulation-induced mitochondrial reactive free oxygen species (MitSOX) in the glioblastoma cells. The aim was to elucidate the effects of CSP and MLT combination via the TRPM2 stimulation on the tumor cell viability, cell number, cell death (propidium iodide/Hoechst rate), apoptosis, and MitSOX levels in the DBTRG-05MG cells.

Silver nanoparticles potentiate antitumor and oxidant actions of cisplatin via the stimulation of TRPM2 channel in glioblastoma tumor cells.

We investigated the effects of silver nanoparticle (AgNP) and cisplatin (CiSP) exposure via the activation of TRPM2 cation channels in glioblastoma (DBTRG-05MG) cell line. The cells were divided into four groups as control, AgNPs (100 μg/ml for 48 h), CiSP (25 μM for 24 h), and CiSP + AgNPs. We found that the cytotoxic, oxidant and apoptotic actions of CiSP were further stimulated through the activation of TRPM2 (via ADP-ribose and HO) in the cells by the treatment of AgNPs.

Agomelatine attenuates calcium signaling and apoptosis via the inhibition of TRPV1 channel in the hippocampal neurons of rats with chronic mild stress depression model.

Chronic stress plays a key role in inducing various clinical disorders through mechanistic pathways, including oxidative stress and apoptosis. Transient receptor potential vanilloid 1 (TRPV1) channels, which are permeable to cations, mainly Ca, are susceptible to oxidative stress. Agomelatine (AGOM) is an antidepressant drug analogous to the antioxidant melatonin hormone, although its action has not been fully clarified yet.

TRPM2 Channel Inhibition Attenuates Amyloid β42-Induced Apoptosis and Oxidative Stress in the Hippocampus of Mice.

Alzheimer's disease (AD) is characterized by the increase of hippocampal Ca influx-induced apoptosis and mitochondrial oxidative stress (OS). The OS is a stimulator of TRPM2, although N-(p-amylcinnamoyl)anthranilic acid (ACA), 2-aminoethyl diphenylborinate (2/APB), and glutathione (GSH) are non-specific antagonists of TRPM2. In the present study, we investigated the protective roles of GSH and TRPM2 antagonist treatments on the amyloid β42 peptide (Aβ)-caused oxidative neurotoxicity and apoptosis in the hippocampus of mice with AD model.

TRPV1 stimulation increased oxidative neurotoxicity and apoptosis in the glia cell membrane but not in the perinuclear area: An evidence of TRPV1 subtype.

Glia are essential neurons of the immune system in the central nervous system. The effective mission of glia depends on their activation, release of cytokines, and oxidative cleaning of debris material from neuronal cells. Accumulating evidence indicates that microglia activation-induced oxidative stress via the activation Ca permeable TRPV1 channel has an essential role in the pathophysiology of neurodegenerative diseases.

Carvacrol protects the ARPE19 retinal pigment epithelial cells against high glucose-induced oxidative stress, apoptosis, and inflammation by suppressing the TRPM2 channel signaling pathways.

Purpose: The concentration of plasma high glucose (HGu) in diabetes mellitus (DM) induces the retinal pigment epithelial cell (ARPE19) death via the increase of inflammation, cytosolic (cytROS), and mitochondrial (mitROS) free oxygen radical generations. Transient potential melastatin 2 (TRPM2) cation channel is stimulated by cytROS and mitROS. Hence, the cytROS and mitROS-mediated excessive Ca influxes via the stimulation of TRPM2 channel cause to the induction of DM-mediated retina oxidative cytotoxicity.

Rituximab Attenuated Lipopolysaccharide-Induced Oxidative Cytotoxicity, Apoptosis, and Inflammation in the Human Retina Cells via Modulating the TRPM2 Signaling Pathways.

Purpose: We investigated the possible protective effects of rituximab (RTX) on LPS-induced oxidant, inflammatory, and apoptotic adverse actions via the inhibition of TRPM2 channel in the adult retinal pigment epithelial-19 (ARPE-19) cells.

Methods: In the cultured ARPE-19 cells, we induced five main groups as control, RTX (10 μg/ml), LPS (1 μg/ml), LPS+RTX, and LPS+TRPM2 blockers (ACA or 2/APB).

Results: The levels of apoptosis, cell death, mitochondrial free reactive oxygen radicals (mitROS), cytosolic ROS, lipid peroxidation, caspase -3, caspase -8, caspase -9, ADP-ribose-induced TRPM2 current density, TNF-α, IL-1β, cytosolic free Zn, and Ca were increased by LPS, although their levels were diminished by the treatments of RTX and TRPM2 blockers.

Eicosapentaenoic acid enhanced apoptotic and oxidant effects of cisplatin via activation of TRPM2 channel in brain tumor cells.

Cisplatin (CiSP) induced-overload Ca entry results in the increase of mitochondrial oxidative stress and apoptosis in the cancer cell. TRPM2 cation channel is gated by the cytosolic ADP-ribose (ADPR) and reactive oxygen species (ROS). The high content of polyunsaturated fatty acid (PUFA) in the brain is a main target of ROS.

Selenium and Resveratrol Attenuated Diabetes Mellitus-Mediated Oxidative Retinopathy and Apoptosis via the Modulation of TRPM2 Activity in Mice.

Diabetes mellitus induces optic nerve injury via the excessive generation of mitochondria reactive free oxygen radical (mitROS). TRPM2 channel is activated by mitROS, although it is inhibited by selenium (Se) and resveratrol (RSV). The activation of TRPM2 induces apoptosis and oxidative injury in the optic nerve.

Amantadine Attenuated Hypoxia-Induced Mitochondrial Oxidative Neurotoxicity, Apoptosis, and Inflammation via the Inhibition of TRPM2 and TRPV4 Channels.

The hypoxia (HPX) acts the brain injury and apoptosis via the Ca influx-induced excessive mitochondria free reactive oxygen species (mitROS) in neurons. The effective treatment of HPX is not possible yet. In addition to the antiviral and antiparkinsonian actions, amantadine (AMN) has been evaluated as a drug in treatments against brain injury.

Paclitaxel Promotes Oxidative Stress-Mediated Human Laryngeal Squamous Tumor Cell Death through the Stimulation of Calcium and Zinc Signaling Pathways: No Synergic Action of Melatonin.

The paclitaxel (PAX) and melatonin (MLT)-mediated mitochondria reactive free oxygen radical (miROS) generations via the influx of excessive Ca and Zn induce tumor cell death and apoptosis. However, a presence of resistance was demonstrated against the PAX treatment in the tumor cells. The stimulation of TRPM2 may increase the anticancer action of PAX after the treatment of MLT.

The involvement of TRPM2 on the MPP-induced oxidative neurotoxicity and apoptosis in hippocampal neurons from neonatal mice: protective role of resveratrol.

Parkinson's disease (PD) is an age-related chronic neurodegenerative disease. Although PD is known to be a result of damage to hippocampal neurons, its molecular mechanism has yet to be completely clarified. The neurodegeneration in hippocampal neurons has been suggested to include excessive production of reactive oxygen species (ROS).