The Experts below are selected from a list of 285 Experts worldwide ranked by ideXlab platform

Carla I. Tasca - One of the best experts on this subject based on the ideXlab platform.

  • Guanosine prevents nitroxidative stress and recovers mitochondrial membrane Potential Disruption in hippocampal slices subjected to oxygen/glucose deprivation
    Purinergic signalling, 2016
    Co-Authors: Daniel Tonial Thomaz, Tharine Dal-cim, Wagner C. Martins, Mauricio P. Cunha, Débora Lanznaster, Carla I. Tasca
    Abstract:

    Guanosine, the endogenous guanine nucleoside, prevents cellular death induced by ischemic events and is a promising neuroprotective agent. During an ischemic event, nitric oxide has been reported to either cause or prevent cell death. Our aim was to evaluate the neuroprotective effects of guanosine against oxidative damage in hippocampal slices subjected to an in vitro ischemia model, the oxygen/glucose deprivation (OGD) protocol. We also assessed the participation of nitric oxide synthase (NOS) enzymes activity on the neuroprotection promoted by guanosine. Here, we showed that guanosine prevented the increase in ROS, nitric oxide, and peroxynitrite production induced by OGD. Moreover, guanosine prevented the loss of mitochondrial membrane Potential in hippocampal slices subjected to OGD. Guanosine did not present an antioxidant effect per se. The protective effects of guanosine were mimicked by inhibition of neuronal NOS, but not of inducible NOS. The neuroprotective effect of guanosine may involve activation of cellular mechanisms that prevent the increase in nitric oxide production, possibly via neuronal NOS.

  • guanosine prevents nitroxidative stress and recovers mitochondrial membrane Potential Disruption in hippocampal slices subjected to oxygen glucose deprivation
    Purinergic Signalling, 2016
    Co-Authors: Daniel Tonial Thomaz, Wagner C. Martins, Mauricio P. Cunha, Débora Lanznaster, Tharine Dalcim, Andreza Fabro De Bem, Carla I. Tasca
    Abstract:

    Guanosine, the endogenous guanine nucleoside, prevents cellular death induced by ischemic events and is a promising neuroprotective agent. During an ischemic event, nitric oxide has been reported to either cause or prevent cell death. Our aim was to evaluate the neuroprotective effects of guanosine against oxidative damage in hippocampal slices subjected to an in vitro ischemia model, the oxygen/glucose deprivation (OGD) protocol. We also assessed the participation of nitric oxide synthase (NOS) enzymes activity on the neuroprotection promoted by guanosine. Here, we showed that guanosine prevented the increase in ROS, nitric oxide, and peroxynitrite production induced by OGD. Moreover, guanosine prevented the loss of mitochondrial membrane Potential in hippocampal slices subjected to OGD. Guanosine did not present an antioxidant effect per se. The protective effects of guanosine were mimicked by inhibition of neuronal NOS, but not of inducible NOS. The neuroprotective effect of guanosine may involve activation of cellular mechanisms that prevent the increase in nitric oxide production, possibly via neuronal NOS.

Arthur M Krieg - One of the best experts on this subject based on the ideXlab platform.

  • cpg dna rescues b cells from apoptosis by activating nfκb and preventing mitochondrial membrane Potential Disruption via a chloroquine sensitive pathway
    International Immunology, 1999
    Co-Authors: Dave W Peckham, R F Ashman, Arthur M Krieg
    Abstract:

    Isolated murine splenic B cells gradually undergo spontaneous apoptosis while WEHI-231 B lymphoma cells undergo activation-induced apoptosis. Unmethylated CpG dinucleotides in a particular sequence context (CpG motif) in bacterial DNA or in synthetic oligodeoxynucleotides (CpG DNA) rescue both splenic B cells and WEHI-231 cells from apoptosis, an effect which could Potentially contribute to autoimmune disease. Chloroquine has been used as an effective therapeutic agent for some autoimmune diseases, although the mechanism of action is not clearly understood. Low concentrations of chloroquine (<5 microM) selectively abolished CpG DNA-mediated protection against spontaneous apoptosis of splenic B cells and against anti-IgM-induced apoptosis of WEHI-231 cells without affecting anti-apoptotic activities of anti-CD40 or lipopolsaccharide. CpG DNA effectively prevented mitochondrial membrane Potential Disruption through a chloroquine-sensitive pathway in splenic B cells. Apoptosis protection by CpG DNA was also associated with increased expression of several proto-oncogenes and oncoproteins directly and/or indirectly through a rapid and sustained activation of NFkappaB in splenic B cells and WEHI-231 cells. These effects were also suppressed by chloroquine. Our results suggest that despite the difference in maturation phenotype of splenic B cells and WEHI-231 cells, CpG DNA rescues both from apoptosis by similar pathway, which is blocked at an early step by chloroquine.

  • CpG DNA rescues B cells from apoptosis by activating NFκB and preventing mitochondrial membrane Potential Disruption via a chloroquine-sensitive pathway
    International immunology, 1999
    Co-Authors: Dave W Peckham, R F Ashman, Arthur M Krieg
    Abstract:

    Isolated murine splenic B cells gradually undergo spontaneous apoptosis while WEHI-231 B lymphoma cells undergo activation-induced apoptosis. Unmethylated CpG dinucleotides in a particular sequence context (CpG motif) in bacterial DNA or in synthetic oligodeoxynucleotides (CpG DNA) rescue both splenic B cells and WEHI-231 cells from apoptosis, an effect which could Potentially contribute to autoimmune disease. Chloroquine has been used as an effective therapeutic agent for some autoimmune diseases, although the mechanism of action is not clearly understood. Low concentrations of chloroquine (

Daniel Tonial Thomaz - One of the best experts on this subject based on the ideXlab platform.

  • Guanosine prevents nitroxidative stress and recovers mitochondrial membrane Potential Disruption in hippocampal slices subjected to oxygen/glucose deprivation
    Purinergic signalling, 2016
    Co-Authors: Daniel Tonial Thomaz, Tharine Dal-cim, Wagner C. Martins, Mauricio P. Cunha, Débora Lanznaster, Carla I. Tasca
    Abstract:

    Guanosine, the endogenous guanine nucleoside, prevents cellular death induced by ischemic events and is a promising neuroprotective agent. During an ischemic event, nitric oxide has been reported to either cause or prevent cell death. Our aim was to evaluate the neuroprotective effects of guanosine against oxidative damage in hippocampal slices subjected to an in vitro ischemia model, the oxygen/glucose deprivation (OGD) protocol. We also assessed the participation of nitric oxide synthase (NOS) enzymes activity on the neuroprotection promoted by guanosine. Here, we showed that guanosine prevented the increase in ROS, nitric oxide, and peroxynitrite production induced by OGD. Moreover, guanosine prevented the loss of mitochondrial membrane Potential in hippocampal slices subjected to OGD. Guanosine did not present an antioxidant effect per se. The protective effects of guanosine were mimicked by inhibition of neuronal NOS, but not of inducible NOS. The neuroprotective effect of guanosine may involve activation of cellular mechanisms that prevent the increase in nitric oxide production, possibly via neuronal NOS.

  • guanosine prevents nitroxidative stress and recovers mitochondrial membrane Potential Disruption in hippocampal slices subjected to oxygen glucose deprivation
    Purinergic Signalling, 2016
    Co-Authors: Daniel Tonial Thomaz, Wagner C. Martins, Mauricio P. Cunha, Débora Lanznaster, Tharine Dalcim, Andreza Fabro De Bem, Carla I. Tasca
    Abstract:

    Guanosine, the endogenous guanine nucleoside, prevents cellular death induced by ischemic events and is a promising neuroprotective agent. During an ischemic event, nitric oxide has been reported to either cause or prevent cell death. Our aim was to evaluate the neuroprotective effects of guanosine against oxidative damage in hippocampal slices subjected to an in vitro ischemia model, the oxygen/glucose deprivation (OGD) protocol. We also assessed the participation of nitric oxide synthase (NOS) enzymes activity on the neuroprotection promoted by guanosine. Here, we showed that guanosine prevented the increase in ROS, nitric oxide, and peroxynitrite production induced by OGD. Moreover, guanosine prevented the loss of mitochondrial membrane Potential in hippocampal slices subjected to OGD. Guanosine did not present an antioxidant effect per se. The protective effects of guanosine were mimicked by inhibition of neuronal NOS, but not of inducible NOS. The neuroprotective effect of guanosine may involve activation of cellular mechanisms that prevent the increase in nitric oxide production, possibly via neuronal NOS.

Wagner C. Martins - One of the best experts on this subject based on the ideXlab platform.

  • Guanosine prevents nitroxidative stress and recovers mitochondrial membrane Potential Disruption in hippocampal slices subjected to oxygen/glucose deprivation
    Purinergic signalling, 2016
    Co-Authors: Daniel Tonial Thomaz, Tharine Dal-cim, Wagner C. Martins, Mauricio P. Cunha, Débora Lanznaster, Carla I. Tasca
    Abstract:

    Guanosine, the endogenous guanine nucleoside, prevents cellular death induced by ischemic events and is a promising neuroprotective agent. During an ischemic event, nitric oxide has been reported to either cause or prevent cell death. Our aim was to evaluate the neuroprotective effects of guanosine against oxidative damage in hippocampal slices subjected to an in vitro ischemia model, the oxygen/glucose deprivation (OGD) protocol. We also assessed the participation of nitric oxide synthase (NOS) enzymes activity on the neuroprotection promoted by guanosine. Here, we showed that guanosine prevented the increase in ROS, nitric oxide, and peroxynitrite production induced by OGD. Moreover, guanosine prevented the loss of mitochondrial membrane Potential in hippocampal slices subjected to OGD. Guanosine did not present an antioxidant effect per se. The protective effects of guanosine were mimicked by inhibition of neuronal NOS, but not of inducible NOS. The neuroprotective effect of guanosine may involve activation of cellular mechanisms that prevent the increase in nitric oxide production, possibly via neuronal NOS.

  • guanosine prevents nitroxidative stress and recovers mitochondrial membrane Potential Disruption in hippocampal slices subjected to oxygen glucose deprivation
    Purinergic Signalling, 2016
    Co-Authors: Daniel Tonial Thomaz, Wagner C. Martins, Mauricio P. Cunha, Débora Lanznaster, Tharine Dalcim, Andreza Fabro De Bem, Carla I. Tasca
    Abstract:

    Guanosine, the endogenous guanine nucleoside, prevents cellular death induced by ischemic events and is a promising neuroprotective agent. During an ischemic event, nitric oxide has been reported to either cause or prevent cell death. Our aim was to evaluate the neuroprotective effects of guanosine against oxidative damage in hippocampal slices subjected to an in vitro ischemia model, the oxygen/glucose deprivation (OGD) protocol. We also assessed the participation of nitric oxide synthase (NOS) enzymes activity on the neuroprotection promoted by guanosine. Here, we showed that guanosine prevented the increase in ROS, nitric oxide, and peroxynitrite production induced by OGD. Moreover, guanosine prevented the loss of mitochondrial membrane Potential in hippocampal slices subjected to OGD. Guanosine did not present an antioxidant effect per se. The protective effects of guanosine were mimicked by inhibition of neuronal NOS, but not of inducible NOS. The neuroprotective effect of guanosine may involve activation of cellular mechanisms that prevent the increase in nitric oxide production, possibly via neuronal NOS.

Débora Lanznaster - One of the best experts on this subject based on the ideXlab platform.

  • Guanosine prevents nitroxidative stress and recovers mitochondrial membrane Potential Disruption in hippocampal slices subjected to oxygen/glucose deprivation
    Purinergic signalling, 2016
    Co-Authors: Daniel Tonial Thomaz, Tharine Dal-cim, Wagner C. Martins, Mauricio P. Cunha, Débora Lanznaster, Carla I. Tasca
    Abstract:

    Guanosine, the endogenous guanine nucleoside, prevents cellular death induced by ischemic events and is a promising neuroprotective agent. During an ischemic event, nitric oxide has been reported to either cause or prevent cell death. Our aim was to evaluate the neuroprotective effects of guanosine against oxidative damage in hippocampal slices subjected to an in vitro ischemia model, the oxygen/glucose deprivation (OGD) protocol. We also assessed the participation of nitric oxide synthase (NOS) enzymes activity on the neuroprotection promoted by guanosine. Here, we showed that guanosine prevented the increase in ROS, nitric oxide, and peroxynitrite production induced by OGD. Moreover, guanosine prevented the loss of mitochondrial membrane Potential in hippocampal slices subjected to OGD. Guanosine did not present an antioxidant effect per se. The protective effects of guanosine were mimicked by inhibition of neuronal NOS, but not of inducible NOS. The neuroprotective effect of guanosine may involve activation of cellular mechanisms that prevent the increase in nitric oxide production, possibly via neuronal NOS.

  • guanosine prevents nitroxidative stress and recovers mitochondrial membrane Potential Disruption in hippocampal slices subjected to oxygen glucose deprivation
    Purinergic Signalling, 2016
    Co-Authors: Daniel Tonial Thomaz, Wagner C. Martins, Mauricio P. Cunha, Débora Lanznaster, Tharine Dalcim, Andreza Fabro De Bem, Carla I. Tasca
    Abstract:

    Guanosine, the endogenous guanine nucleoside, prevents cellular death induced by ischemic events and is a promising neuroprotective agent. During an ischemic event, nitric oxide has been reported to either cause or prevent cell death. Our aim was to evaluate the neuroprotective effects of guanosine against oxidative damage in hippocampal slices subjected to an in vitro ischemia model, the oxygen/glucose deprivation (OGD) protocol. We also assessed the participation of nitric oxide synthase (NOS) enzymes activity on the neuroprotection promoted by guanosine. Here, we showed that guanosine prevented the increase in ROS, nitric oxide, and peroxynitrite production induced by OGD. Moreover, guanosine prevented the loss of mitochondrial membrane Potential in hippocampal slices subjected to OGD. Guanosine did not present an antioxidant effect per se. The protective effects of guanosine were mimicked by inhibition of neuronal NOS, but not of inducible NOS. The neuroprotective effect of guanosine may involve activation of cellular mechanisms that prevent the increase in nitric oxide production, possibly via neuronal NOS.