EGb 761 reduces Ca influx and apoptosis after pentylenetetrazole treatment in a neuroblastoma cell line.

Background: Transient receptor potential (TRP) channels have been found to have significant implications in neuronal outgrowth, survival, inflammatory neurogenic pain, and various epileptogenic processes. Moreover, there is a growing body of evidence indicating that transient receptor potential (TRP) channels have a significant impact on epilepsy and its drug-resistant subtypes.

Objective: We postulated that Gb 761 would modulate TRPA1 channels, thereby exhibiting anti-inflammatory and neuroprotective effects in a neuroblastoma cell line.

Protective and Therapeutic Role of Ginkgo Biloba Extract Through TRPV1 Channels in an in Vitro Alzheimer's Disease Model.

Introduction: The effect of Ginkgo biloba (GB) on mitochondria-dependent TRPV1 ion channels in neuroblastoma cells was investigated by creating an Alzheimer's disease (AD) model.

Methods: Okadaic acid was applied on SH-SY5Y cells to create an AD model. After cellular differentiation, the study was organized with the seven main groups, examining the effect of GB on calcium depended TRPV1 channels in neuroblastoma cells AD, has been established in vitro.

Potential Effects of Melatonin on TRPA1 Channels in the Prevention and Treatment of Alzheimer's Disease.

Introduction: Alzheimer's disease (AD) is the most common cause of dementia and is defined as a progressive neurodegenerative disease. Main clinical features of AD are progressive impairment in learning and memory loss. Several studies have indicated that mitochondria play a critical role in the pathogenesis of AD.

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.

Effects of homocysteine and memantine on oxidative stress related TRP cation channels in model of Alzheimer's disease.

Memantine (MEM) has been used to treat patients with Alzheimer' disease though inhibition of reactive oxygen species (ROS), Ca entry and glutamate receptor. The Ca permeable TRPA1, TRPM2 and TRPV1 channels are activated in the hippocampus by ROS, and antioxidant MEM as a potent TRPA1, TRPM2 and TRPV1 channel antagonist may reduce Aβ-induced oxidative stress and apoptosis in the neurons. In the current study, we investigated the neuroprotective properties of MEM in Aβ-induced hippocampal neuron cultures.

LLLT enhance cyclophosphamide induced TRPM2 channel activation in human colon cancer cells.

Aim: Transient receptor potential (TRP) channels expression is enhanced significantly in colon cancer cells and  Low Lever Laser Treatment (LLLT), is known to have effects and is used clinically in the treatment ofmany diseases, including colon cancer. We aimed to reveal the effects of (LLLT) on apoptosis of colon cancer and on the efficacy of cyclophosphamide via Transient receptor potential melastatin 2 (TRPM2) channels.

Method: Human colon cancer cells (Caco-2) were cultured and cells were divided into seven main groups.

Correction to: Selenium enhances TRPA1 channel-mediated activity of temozolomide in SH-SY5Y neuroblastoma cells.

The original version of this article unfortunately contained few errors. The dose of sodium selenite was incorrectly indicated as 100 μM in the published version of "Selenium enhances TRPA1 channel-mediated activity of temozolomide in SH-SY5Y neuroblastoma cells". The correct indication of sodium selenite is 5 µM.

Selenium enhances TRPA1 channel-mediated activity of temozolomide in SH-SY5Y neuroblastoma cells.

Purpose: Neuroblastoma is a malignant solid tumor that originates from the sympathetic nervous system in early childhood. Temozolomide is used for treatment in high-risk groups with low treatment response of neuroblastomas. TRPA1 channels in neuroblastoma cells are calcium permeable channels that can be activated by reactive oxygen species (ROT).

The role of selenium in bevacizumab induced cardiotoxicity.

Objective: We investigated the role of selenium in bevacizumab induced cardiotoxicity and involvement of transient receptor potential vanilloid 1 (TRPV1) channels in cardiomyocytes.

Materials And Methods: All cells (Human cardiomyocyte cell line) were cultured at 37 °C. We divided the cells into seven groups as control, bevacizumab, bevacizumab + capsazepin, bevacizumab + selenium, bevacizumab + selenium + capsazepin, selenium and selenium + capsazepin groups.

Synergic and comparative effect of 5-fluorouracil and leucoverin on breast and colon cancer cells through TRPM2 channels.

Objectives: We aimed to reveal the role of 5-fluorouracil (5-FU) and Leucovorin (LV) along with transient receptor potential protein melastatin 2 (TRPM2) channels in breast and colon cancer cells during the treatment process.

Background: 5-FU and LV are widely used in breast and colon cancers for chemotherapy. It has been reported that the expression of TRPM2 channels increased intensively in cancer cells.

The effect of melatonin on digoxin‑induced cardiac damage in cardiomyocytes.

Objectives: Digoxin is a cardiac glycoside which is widely used in cardiovascular medicine. Oxidative stress, as well as intracellular Ca2+ overload, plays an important role in digoxin toxicity. Transient receptor potential vanilloid 1 (TRPV1) channels are found in cardiomyocyte cells and they are activated by reactive oxygen species.

Corrigendum: The neuroprotective action of dexmedetomidine on apoptosis, calcium entry and oxidative stress in cerebral ischemia-induced rats: Contribution of TRPM2 and TRPV1 channels.

This corrects the article DOI: 10.1038/srep37196.

Zoledronic Acid, Bevacizumab and Dexamethasone-Induced Apoptosis, Mitochondrial Oxidative Stress, and Calcium Signaling Are Decreased in Human Osteoblast-Like Cell Line by Selenium Treatment.

Increased intracellular free calcium ion (Ca) concentration induces excessive oxidative stress and apoptosis. Medical procedures such as zoledronic acid (Zol), bevacizumab (Bev), and dexamethasone (Dex) are usually used in the treatment of bone diseases (osteoporosis, Paget's disease, etc.) and to prevent metastasis in the bone although the procedures induce osteonecrosis of the jaw through excessive production of reactive oxygen species (ROS).

Hypericum perforatum L. supplementation protects sciatic nerve injury-induced apoptotic, inflammatory and oxidative damage to muscle, blood and brain in rats.

Objectives: This study was conducted to explore whether Hypericum perforatum L. (HPL) as a potent antioxidant protects against oxidative stress, cytokine production and caspase expression in muscle (soleus), brain and blood of sciatic nerve injury (SNI)-induced rats.

Methods: Thirty-five rats were equally divided into five groups.

The neuroprotective action of dexmedetomidine on apoptosis, calcium entry and oxidative stress in cerebral ischemia-induced rats: Contribution of TRPM2 and TRPV1 channels.

Dexmedetomidine (DEX) may act as an antioxidant through regulation of TRPM2 and TRPV1 channel activations in the neurons by reducing cerebral ischemia-induced oxidative stress and apoptosis. The neuroprotective roles of DEX were tested on cerebral ischemia (ISC) in the cultures of rat primary hippocampal and DRG neurons. Fifty-six rats were divided into five groups.

Selenium attenuates apoptosis, inflammation and oxidative stress in the blood and brain of aged rats with scopolamine-induced dementia.

A potent antioxidant, selenium might modulate dementia-induced progression of brain and blood oxidative and apoptotic injuries. The present study explores whether selenium protects against experimental dementia (scopolamine, SCOP)-induced brain, and blood oxidative stress, apoptosis levels, and cytokine production in rats. Thirty-two rats were equally divided into four groups.

Duloxetine Reduces Oxidative Stress, Apoptosis, and Ca Entry Through Modulation of TRPM2 and TRPV1 Channels in the Hippocampus and Dorsal Root Ganglion of Rats.

Overload of Ca entry and excessive oxidative stress in neurons are the two main causes of depression. Activation of transient receptor potential (TRP) vanilloid type 1 (TRPV1) and TRP melastatin 2 (TRPM2) during oxidative stress has been linked to neuronal survival. Duloxetine (DULOX) in neurons reduced the effects of Ca entry and reactive oxygen species (ROS) through glutamate receptors, and this reduction of effects may also occur through TRPM2 and TRPV1 channels.

Raloxifene and Tamoxifen Reduce PARP Activity, Cytokine and Oxidative Stress Levels in the Brain and Blood of Ovariectomized Rats.

It is well known that 17β-estradiol (E2) has an antioxidant role on neurological systems in the brain. Raloxifene (RLX) and tamoxifen (TMX) are selective estrogen receptor modulators. An E2 deficiency stimulates mitochondrial functions for promoting apoptosis and increasing reactive oxygen species (ROS) production.

Selenium potentiates the anticancer effect of cisplatin against oxidative stress and calcium ion signaling-induced intracellular toxicity in MCF-7 breast cancer cells: involvement of the TRPV1 channel.

Background: In breast cancers, calcium signaling is a main cause of proliferation and apoptosis of breast cancer cells. Although previous studies have implicated the transient receptor potential vanilloid 1 (TRPV1) cation channel, the synergistic inhibition effects of selenium (Se) and cisplatin in cancer and the suppression of ongoing apoptosis have not yet been investigated in MCF-7 breast cancer cells. This study investigates the anticancer properties of Se through TRPV1 channel activity in MCF-7 breast cancer cell line cultures when given alone or in combination with cisplatin.

The Protective Role of Selenium on Scopolamine-Induced Memory Impairment, Oxidative Stress, and Apoptosis in Aged Rats: The Involvement of TRPM2 and TRPV1 Channels.

Inhibition of Ca entry into the hippocampus and dorsal root ganglion (DRG) through inhibition of N-methyl-D-aspartate (NMDA) receptor antagonist drugs is the current standard of care in neuronal diseases such as Alzheimer's disease, dementia, and peripheral pain. Oxidative stress activates Ca-permeable TRPM2 and TRPV1, and recent studies indicate that selenium (Se) is a potent TRPM2 and TRPV1 channel antagonist in the hippocampus and DRG. In this study, we investigated the neuroprotective properties of Se in primary hippocampal and DRG neuron cultures of aged rats when given alone or in combination with scopolamine (SCOP).

Modulation of Diabetes-Induced Oxidative Stress, Apoptosis, and Ca Entry Through TRPM2 and TRPV1 Channels in Dorsal Root Ganglion and Hippocampus of Diabetic Rats by Melatonin and Selenium.

Neuropathic pain and hippocampal injury can arise from the overload of diabetes-induced calcium ion (Ca) entry and oxidative stress. The transient receptor potential (TRP) melastatin 2 (TRPM2) and TRP vanilloid type 1 (TRPV1) are expressed in sensory neurons and hippocampus. Moreover, activations of TRPM2 and TRPV1 during oxidative stress have been linked to neuronal death.

Short-Term Ketamine Treatment Decreases Oxidative Stress Without Influencing TRPM2 and TRPV1 Channel Gating in the Hippocampus and Dorsal Root Ganglion of Rats.

Calcium ions (Ca) are important second messengers in neurons. Ketamine (KETAM) is an anesthetic and analgesic, with psychotomimetic effects and abuse potential. KETAM modulates the entry of Ca in neurons through glutamate receptors, but its effect on transient receptor potential melastatin 2 (TRPM2) and transient receptor potential vanilloid 1 (TRPV1) channels has not been clarified.

Synergic Effects of Doxorubicin and Melatonin on Apoptosis and Mitochondrial Oxidative Stress in MCF-7 Breast Cancer Cells: Involvement of TRPV1 Channels.

Transient receptor transient receptor potential vanilloid 1 (TRPV1) is a Ca(2+)-permeable channel gated by oxidative stress and capsaicin (CAP) and modulated by melatonin (MEL) and capsazepine (CPZ). A combination of doxorubicin (DOX) and MEL may offer a potential therapy for breast cancer by exerting antitumor and anti-apoptotic effects and modulating Ca(2+) influx and TRPV1 activity. We aimed to investigate the effects of MEL and DOX on the oxidative toxicity of MCF-7 human breast cancer cells, in addition to the activity of the TRPV1 channel and apoptosis.

Involvement of apoptosis and calcium accumulation through TRPV1 channels in neurobiology of epilepsy.

Calcium ion accumulation into the cytosol of the hippocampus and dorsal root ganglion (DRG) are main reasons in etiology of epilepsy. Transient receptor potential vanilloid type 1 (TRPV1) channel is a cation-permeable calcium channel found in the DRG and hippocampus. Although previous studies implicate TRPV1 channels in the generation of epilepsy, suppression of ongoing seizures by TRPV1 antagonists has not yet been investigated.

Homocysteine and cytosolic GSH depletion induce apoptosis and oxidative toxicity through cytosolic calcium overload in the hippocampus of aged mice: involvement of TRPM2 and TRPV1 channels.

Oxidative stress and apoptosis were induced in neuronal cultures by inhibition of glutathione (GSH) biosynthesis with d,l-buthionine-S,R-sulfoximine (BSO). Transient receptor potential melastatin 2 (TRPM2) and transient receptor potential vanilloid 1 (TRPV1) cation channels are gated by oxidative stress. The oxidant effects of homocysteine (Hcy) may induce activation of TRPV1 and TRPM2 channels in aged mice as a model of Alzheimer's disease (AD).