Search

WOS: 000530579900004 PubMed: 32356430 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. Cells were incubated with cyclophosphamide, TRPM2 channel inhibitor, stimulator and low level laser exposure separately and together. The effects of cyclophosphamide and low level laser were investigated on apoptosis. RESULTS: It was found that the levels of apoptosis in cyclophosphamide group were significantly increased in cancer cells compared to the control group. TRPM2 channel stimulator administration resulted in significantly increased apoptosis levels compared to the control group, in cyclophosphamide + low level laser group the apoptosis level was significantly increased compared to the cyclophosphamide-only group. CONCLUSIONS: It has been shown that apoptotic effects of cyclophosphamide on colon cancer cells were directly related to TRPM2 channels, low level laser increased apoptosis in colon cancer cells through TRPM2 channels and induced apoptotic effect of cyclophosphamide (Fig. 5, Ref. 26).

Aim: Paclitaxel is widely used in adjuvant treatment of early breast cancer and second-line treatment of metastatic breast cancer. It has been reported that transient receptor potential melastatin-2 (TRPM2) channels are expressed intensively in breast cancer and has significant effects on oxidative stress. Selenium is an essential element and has effects on reproduction, toxicity, antiaging and DNA reproduction. In this study, we aimed to reveal the role of selenium and TRPM2 channels on apoptotic effects of paclitaxel in breast cancer cells. Material and Methods: Breast cancer cells (MCF-7) were cultured and cells were divided into seven main groups. Cells were incubated with paclitaxel and selenium separately and together administrated on breast cancer cell cultures. Cell cultures incubated with TRPM2 channel antagonist anthranilic acid and stimulator cumene-hydroperoxyde. The effects of paclitaxel and selenium were invastigated on molecular pathways of apoptosis. Results: It was found that the levels of apoptosis in paclitaxel group were significantly increased in cancer cells compared to control group (p

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 first and second were used as untreated control and sham control groups, respectively. The third, fourth and fifth were sham + HPL, SNI and SNI + HPL groups, respectively. The third and fifth groups received 30 mg/kg HPL via gastric gavage for 28 days. Key findings High levels of muscle, brain and red blood cell (RBC) lipid peroxidation, plasma cytokine (TNF-α, IL-1β and IL-2), muscle PARP, caspase 3 and 9 expression levels were decreased by HPL treatments. Plasma glutathione peroxidase (GPx) activity, α-tocopherol and melatonin, muscle, brain and RBC reduced glutathione (GSH) concentrations were decreased by SNI induction, whereas their values were increased by HPL treatments. β-carotene and retinol concentrations did not change in the five groups. Conclusion HPL may play a role in preventing SNI-induced inflammatory, oxidative and apoptotic blood, muscle and brain damages through upregulation of the GSH and GPx values but downregulation of PARP, caspase level and cytokine production in SNI-induced rats.

Amaç: Imatinib mesilat bir tirozin kinaz inhibitörüdür ve kronik miyeloid löseminin standart bir birinci basamak tedavisi olarak onaylanmıştır. Kemoterapiye bağlı kardiyotoksisitede oksidatif stresin yanı sıra hücre içi kalsiyum aşırı yüklenmesi ve mitokondriyal disfonksiyon önemli rol oynar. İmatinib ile indüklenen kardiyotoksisitenin neden olduğu altta yatan patofizyolojik mekanizma tam olarak anlaşılamamıştır. Bu çalışmada, geçici reseptör potansiyel melastatin 2 (TRPM2) kanalları üzerinden kalsiyum akışı, oksidatif stres ve apoptozdaki değişimleri araştırdık. Ayrıca, imatinib mesilat kaynaklı kardiyotoksisite sırasında astaksantinin kardiyomiyositlerde modülatör rolü olup olmadığını araştırdık.Gereç ve yöntemler: Hücreler, kontrol, imatinib, imatinib + antranilik asit, imatinib + astaksantin, imatinib + antranilik asit + astaksantin, astaksantin ve astaksantin + antranilik asit grupları olmak üzere yedi ana gruba ayrıldı. Gruplardaki hücreler, ilgili deneylerde TRPM2 kanallarının aktivasyonu ve inaktivasyonu için sırasıyla kümen hidroperoksit ile uyarıldı ve antranilik asit ile inhibe edildi. Sitosolik kalsiyum, hücre içi reaktif oksijen, mitokondriyal depolarizasyon, kaspaz 3 ve kaspaz 9 seviyeleri ölçüldü.Bulgular: Apoptoz değerleri astaksantin ve imatinib + astaksantin grubunda, imatinib grubundaki kardiyomiyositlerden anlamlı olarak daha düşüktü (p, Aim: Imatinib mesylate is a tyrosine kinase inhibitor and is approved as a standard first-line therapy of chronic myeloid leukemia. Oxidative stress, as well as intracellular calcium overload and mitochondrial dysfunction, play an important role in chemotherapy-induced cardiotoxicity. The underlying pathophysiological mechanism associated with imatinib-induced cardiotoxicity is not well understood. In the present study, we investigated alterations in calcium influx, oxidative stress and apoptosis through transient receptor potential melastatin 2 (TRPM2) channels. Also, we aimed to investigate if there is a modulator role of astaxanthin in cardiomyocytes during imatinib mesylate-induced cardiotoxicity. Materials and methods: The cells were divided into seven main control groups: imatinib, imatinib+antranilic acid, imatinib+astaxanthin, imatinib+antranilic acid+astaxanthin, astaxanthin and astaxanthin+antranilic acid groups. Cells in the groups were stimulated with cumene hydroperoxide and inhibited with antranilic acid in related experiments for activation and inactivation of TRPM2 channels, respectively. We measured cytosolic calcium, intracellular reactive oxygene, mitochondrial depolarization, caspase 3 and caspase 9 levels.Results: The apoptosis values were significantly lower in the astaxanthin and the imatinib+astaxanthin group than in the imatinib group of cardiomyocytes (p< 0.001). The cell viability values were significantly higher in the imatinib+astaxanthin+antranilic acid (p

Calcium ions (Ca2+) are important second messengers in neurons. Ketamine (KETAM) is an anesthetic and analgesic, with psychotomimetic effects and abuse potential. KETAM modulates the entry of Ca2+ 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. This study investigated the short-term effects of KETAM on oxidative stress and TRPM2 and TRPV1 channel gating in hippocampal and dorsal root ganglion (DRG) neurons of rats. Freshly isolated hippocampal and DRG neurons were incubated for 24 h with KETAM (0.3 mM). The TRPM2 channel antagonist, N-(p-amylcinnamoyl)anthranilic acid (ACA), inhibited cumene hydroperoxide and ADP-ribose-induced TRPM2 currents in the neurons, and capsazepine (CPZ) inhibited capsaicin-induced TRPV1 currents. The TRPM2 and TRPV1 channel current densities and intracellular free calcium ion concentration of the neurons were lower in the neurons exposed to ACA and CPZ compared to the control neurons, respectively. However, the values were not further decreased by the KETAM + CPZ and KETAM + ACA treatments. KETAM decreased lipid peroxidation levels in the neurons but increased glutathione peroxidase activity. In conclusion, short-term KETAM treatment decreased oxidative stress levels but did not seem to influence TRPM2- and TRPV1-mediated Ca2+ entry.

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. Additionally the authors accidenttally referred to reference 11 instead of reference 10 in Group 6.

Aim : 5-fluorouracil has been widely used in breast cancer treatment. Low level laser therapy (LLLT) has been shown to modulate biological processes and used in cancer treatment. It has been reported that apoptosis is induced by stimulation of transient receptor potential protein channels in numerous cancer cells, including breast cancer. We aimed to reveal the effects of 5-fluorouracil / Leucovorin (5-FU/LV) and . low level laser on apoptosis via transient receptor protein ancyrin 1 (TRPA1) channels. Material and Methods: Breast cancer cells (MCF-7) were cultured and cells were divided into seven main groups. Cells were incubated with 5-FU/LV and LLLT exposure separately and together performed on MCF-7 cell cultures. Cell cultures incubated with TRPV1 channel antagonist capsazepin and stimulator capsaicin. The effects of 5-FU and LLLT were investigated on all molecular pathways of apoptosis. Results: It was found that the levels of apoptosis in 5-FU/LV group were significantly increased in cancer cells compared to control group .TRPA1 channel stimulator administration resulted in significantly increased apoptosis levels compared to the control group, in 5-FU/LV + low level laser group the apoptosis level significantly reduced compared to 5-FU/LV-only group. (p

Scientific Reports 6; Article number: 37196; published online: 22 November 2016; updated: 04 July 2018 In this Article, the legend of Figure 2 contains errors. The two instances of ‘TRPM2’ should read ‘TRPV1’. Figure 3 contains errors. Figure 3c was inadvertently duplicated from Figure 4c. Figure 3eis incorrect.

Transient Receptor Potential (TRP) channels superfamily has mostly calcium ion (Ca2+) permeable non-selective cation channels. Transient receptor potential melastatin subfamily 2 (TRPM2) is widely expressed in central nervous system. Intracellular Ca2+ concentration ([Ca2+]i) may change depend on TRPM2 and TRPM8 activations from extracellular liquid to cytosol. Curcumin as natural antioxidant shows phenolic structure, synthesized by Curcuma longa L. (Indian saffron, turmeric), has powerful non-enzymatically antioxidant effects. Low dose curcumin treatment can decrease calcium signaling via TRPM2 channel inhibition and prevent elevation of [Ca2+]i levels. Hence, we investigated effects of four different concentrations (5, 10, 25 and 50 µM) of curcumin on apoptosis and cell viability (MTT), reactive oxygen species (ROS) production, mitochondrial membrane potential levels, caspase 3 and caspase 9 values in DBRG glioblastoma cells. We found that curcumin reduces cell viability by concentration dependent manner. It was also observed that curcumin induces apoptosis via caspase 3 and 9 related pathways. However, it was not found any direct relationship between the effect of increased concentrations of curcumin and inhibition or activation of TRPM2 mediated Ca2+ signaling in the DBTRG cells. The [Ca2+]i concentration was lower in 5 µM group as compare to control group. Curcumin acted important role on decrease of mitochondrial membrane potential and intracellular ROS production in the cells. Moreover, curcumin treatment markedly supported GSH concentration levels in the cells. In conclusion, it was firstly assessed the effects of different doses of curcumin on TRPM2 mediated calcium signaling and interaction with various apoptosis parameters in DBTRG glioblastoma cells.

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. A placebo was given to control, sham control, and ISC groups, respectively. In the third group, ISC was induced. The DEX and ISC+DEX groups received intraperitoneal DEX (40 μg/kg) 3, 24, and 48 hours after ISC induction. DEX effectively reversed capsaicin and cumene hydroperoxide/ADP-ribose-induced TRPV1 and TRPM2 densities and cytosolic calcium ion accumulation in the neurons, respectively. In addition, DEX completely reduced ISC-induced oxidative toxicity and apoptosis through intracellular reactive oxygen species production and depolarization of mitochondrial membrane. The DEX and ISC+DEX treatments also decreased the expression levels of caspase 3, caspase 9, and poly (ADP-ribose) polymerase in the hippocampus and DRG. In conclusion, the current results are the first to demonstrate the molecular level effects of DEX on TRPM2 and TRPV1 activation. Therefore, DEX can have remarkable neuroprotective impairment effects in the hippocampus and DRG of ISC-induced rats.