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Difference between revisions of "Jing 2015 Int J Biol Sci"

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{{Publication
{{Publication
|title=Jing L, He MT, Chang Y, Mehta SL, He QP, Zhang JZ, Li PA (2014) Coenzyme Q10 protects astrocytes from ROS-induced damage through Inhibition of mitochondria-mediated cell death pathway. Int J Biol Sci 11:59-66.
|title=Jing L, He MT, Chang Y, Mehta SL, He QP, Zhang JZ, Li PA (2015) Coenzyme Q10 protects astrocytes from ROS-induced damage through inhibition of mitochondria-mediated cell death pathway. Int J Biol Sci 11:59-66.
|info=[http://www.ncbi.nlm.nih.gov/pubmed/25552930 PMID:25552930 Open Acess]
|authors=Jing L, He MT, Chang Y, Mehta SL, He QP, Zhang JZ, Li PA
|authors=Jing L, He MT, Chang Y, Mehta SL, He QP, Zhang JZ, Li PA
|year=2014
|year=2015
|journal=Int J Biol Sci
|journal=Int J Biol Sci
|abstract=Coenzyme Q10 (CoQ10) acts by scavenging reactive oxygen species to protect neuronal cells against oxidative stress in neurodegenerative diseases. The present study was designed to examine whether CoQ10 was capable of protecting astrocytes from reactive oxygen species (ROS) mediated damage. For this purpose, ultraviolet B (UVB) irradiation was used as a tool to induce ROS stress to cultured astrocytes. The cells were treated with 10 and 25 ฮผg/ml of CoQ10 for 3 or 24 h prior to the cells being exposed to UVB irradiation and maintained for 24 h post UVB exposure. Cell viability was assessed by MTT conversion assay. Mitochondrial respiration was assessed by respirometer. While superoxide production and mitochondrial membrane potential were measured using fluorescent probes, levels of cytochrome C (cyto-c), cleaved caspase-9, and caspase-8 were detected using Western blotting and/or immunocytochemistry. The results showed that UVB irradiation decreased cell viability and this damaging effect was associated with superoxide accumulation, mitochondrial membrane potential hyperpolarization, mitochondrial respiration suppression, cyto-c release, and the activation of both caspase-9 and -8. Treatment with CoQ10 at two different concentrations started 24 h before UVB exposure significantly increased the cell viability. The protective effect of CoQ10 was associated with reduction in superoxide, normalization of mitochondrial membrane potential, improvement of mitochondrial respiration, inhibition of cyto-c release, suppression of caspase-9. Furthermore, CoQ10 enhanced mitochondrial biogenesis. It is concluded that CoQ10 may protect astrocytes through suppression of oxidative stress, prevention of mitochondrial dysfunction, blockade of mitochondria-mediated cell death pathway, and enhancement of mitochondrial biogenesis.
|abstract=Coenzyme Q10 (CoQ10) acts by scavenging reactive oxygen species to protect neuronal cells against oxidative stress in neurodegenerative diseases. The present study was designed to examine whether CoQ10 was capable of protecting astrocytes from reactive oxygen species (ROS) mediated damage. For this purpose, ultraviolet B (UVB) irradiation was used as a tool to induce ROS stress to cultured astrocytes. The cells were treated with 10 and 25 ฮผg/ml of CoQ10 for 3 or 24 h prior to the cells being exposed to UVB irradiation and maintained for 24 h post UVB exposure. Cell viability was assessed by MTT conversion assay. Mitochondrial respiration was assessed by respirometer. While superoxide production and mitochondrial membrane potential were measured using fluorescent probes, levels of cytochrome C (cyto-c), cleaved caspase-9, and caspase-8 were detected using Western blotting and/or immunocytochemistry. The results showed that UVB irradiation decreased cell viability and this damaging effect was associated with superoxide accumulation, mitochondrial membrane potential hyperpolarization, mitochondrial respiration suppression, cyto-c release, and the activation of both caspase-9 and -8. Treatment with CoQ10 at two different concentrations started 24 h before UVB exposure significantly increased the cell viability. The protective effect of CoQ10 was associated with reduction in superoxide, normalization of mitochondrial membrane potential, improvement of mitochondrial respiration, inhibition of cyto-c release, suppression of caspase-9. Furthermore, CoQ10 enhanced mitochondrial biogenesis. It is concluded that CoQ10 may protect astrocytes through suppression of oxidative stress, prevention of mitochondrial dysfunction, blockade of mitochondria-mediated cell death pathway, and enhancement of mitochondrial biogenesis.
|keywords=Astrocyte, Caspase, Coenzyme Q10, Mitochondrion, Reactive oxygen species, Ultraviolet
|keywords=Astrocyte, Caspase, Coenzyme Q10, Mitochondrion, Reactive oxygen species, Ultraviolet
|mipnetlab=US NC Durham Li AP
|mipnetlab=US NC Durham Li PA
}}
}}
{{Labeling
{{Labeling
|area=Respiration
|area=Respiration
|organism=Human
|injuries=Oxidative stress;RONS
|tissues=Nervous system
|organism=Mouse
|model cell lines=Other cell lines
|tissues=Nervous system, Other cell lines
|preparations=Homogenate
|preparations=Homogenate
|injuries=RONS; Oxidative Stress
|instruments=Oxygraph-2k
|instruments=Oxygraph-2k
}}
}}

Latest revision as of 09:49, 9 November 2016

Publications in the MiPMap
Jing L, He MT, Chang Y, Mehta SL, He QP, Zhang JZ, Li PA (2015) Coenzyme Q10 protects astrocytes from ROS-induced damage through inhibition of mitochondria-mediated cell death pathway. Int J Biol Sci 11:59-66.

ยป PMID:25552930 Open Acess

Jing L, He MT, Chang Y, Mehta SL, He QP, Zhang JZ, Li PA (2015) Int J Biol Sci

Abstract: Coenzyme Q10 (CoQ10) acts by scavenging reactive oxygen species to protect neuronal cells against oxidative stress in neurodegenerative diseases. The present study was designed to examine whether CoQ10 was capable of protecting astrocytes from reactive oxygen species (ROS) mediated damage. For this purpose, ultraviolet B (UVB) irradiation was used as a tool to induce ROS stress to cultured astrocytes. The cells were treated with 10 and 25 ฮผg/ml of CoQ10 for 3 or 24 h prior to the cells being exposed to UVB irradiation and maintained for 24 h post UVB exposure. Cell viability was assessed by MTT conversion assay. Mitochondrial respiration was assessed by respirometer. While superoxide production and mitochondrial membrane potential were measured using fluorescent probes, levels of cytochrome C (cyto-c), cleaved caspase-9, and caspase-8 were detected using Western blotting and/or immunocytochemistry. The results showed that UVB irradiation decreased cell viability and this damaging effect was associated with superoxide accumulation, mitochondrial membrane potential hyperpolarization, mitochondrial respiration suppression, cyto-c release, and the activation of both caspase-9 and -8. Treatment with CoQ10 at two different concentrations started 24 h before UVB exposure significantly increased the cell viability. The protective effect of CoQ10 was associated with reduction in superoxide, normalization of mitochondrial membrane potential, improvement of mitochondrial respiration, inhibition of cyto-c release, suppression of caspase-9. Furthermore, CoQ10 enhanced mitochondrial biogenesis. It is concluded that CoQ10 may protect astrocytes through suppression of oxidative stress, prevention of mitochondrial dysfunction, blockade of mitochondria-mediated cell death pathway, and enhancement of mitochondrial biogenesis. โ€ข Keywords: Astrocyte, Caspase, Coenzyme Q10, Mitochondrion, Reactive oxygen species, Ultraviolet

โ€ข O2k-Network Lab: US NC Durham Li PA


Labels: MiParea: Respiration 

Stress:Oxidative stress;RONS  Organism: Mouse  Tissue;cell: Nervous system, Other cell lines  Preparation: Homogenate 



HRR: Oxygraph-2k