1,5-Dicaffeoylquinic acid-mediated glutathione synthesis through activation of Nrf2 protects against OGD/reperfusion-induced oxidative stress in astrocytes

Xu Cao; Haibing Xiao; Ying Zhang; Liangyu Zou; Yinghao Chu; Xiaofan Chu

doi:10.1016/j.brainres.2010.05.072

1,5-Dicaffeoylquinic acid-mediated glutathione synthesis through activation of Nrf2 protects against OGD/reperfusion-induced oxidative stress in astrocytes

Xu Cao, Haibing Xiao, Ying Zhang, Liangyu Zou, Yinghao Chu, Xiaofan Chu

Research output: Journal Publications and Reviews › RGC 21 - Publication in refereed journal › peer-review

47 Citations (Scopus)

Abstract

Oxidative stress plays an important role in pathological processes of cerebral ischemia followed by reperfusion. The effect of 1, 5-dicaffeoylquinic acid (1, 5-diCQA) on primary culture rat cortical astrocytes induced by oxygen and glucose deprivation (OGD)/reperfusion was evaluated in this study. Appropriate concentration of 1, 5-diCQA pretreatment significantly suppressed cell death, reduced the production of reactive oxygen species, prevented glutathione (GSH) depletion, increased the activity of glutamate-cysteine ligase (GCL), and triggered Nrf2 nuclear translocation in astrocytes induced by 4 h of OGD and 20 h of reperfusion. Interestingly, these protective effects were greatly attenuated in Nrf2 siRNA-transfected cells. We conclude that 1, 5-diCQA has antioxidant signaling properties that upregulate GSH synthesis by stimulating the Nrf2 pathway in astrocytes and protects them from cell death in an in vitro model of ischemia/reperfusion. © 2010 Elsevier B.V. All rights reserved.

Original language	English
Pages (from-to)	142-148
Journal	Brain Research
Volume	1347
DOIs	https://doi.org/10.1016/j.brainres.2010.05.072
Publication status	Published - 6 Aug 2010
Externally published	Yes

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Publication details (e.g. title, author(s), publication statuses and dates) are captured on an “AS IS” and “AS AVAILABLE” basis at the time of record harvesting from the data source. Suggestions for further amendments or supplementary information can be sent to [email protected].

Funding

This work was supported by grants from the National Natural Science Foundation of China (grant numbers 30971024 and 30870845) and the Guangdong Provincial Natural Science Foundation (grant number 91510515000009).

Research Keywords

1,5-Dicaffeoylquinic acid
Glutathione
Ischemia/reperfusion
Nrf2
Oxidative stress

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abstract = "Oxidative stress plays an important role in pathological processes of cerebral ischemia followed by reperfusion. The effect of 1, 5-dicaffeoylquinic acid (1, 5-diCQA) on primary culture rat cortical astrocytes induced by oxygen and glucose deprivation (OGD)/reperfusion was evaluated in this study. Appropriate concentration of 1, 5-diCQA pretreatment significantly suppressed cell death, reduced the production of reactive oxygen species, prevented glutathione (GSH) depletion, increased the activity of glutamate-cysteine ligase (GCL), and triggered Nrf2 nuclear translocation in astrocytes induced by 4 h of OGD and 20 h of reperfusion. Interestingly, these protective effects were greatly attenuated in Nrf2 siRNA-transfected cells. We conclude that 1, 5-diCQA has antioxidant signaling properties that upregulate GSH synthesis by stimulating the Nrf2 pathway in astrocytes and protects them from cell death in an in vitro model of ischemia/reperfusion. {\textcopyright} 2010 Elsevier B.V. All rights reserved.",

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AU - Zou, Liangyu

AU - Chu, Yinghao

AU - Chu, Xiaofan

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N2 - Oxidative stress plays an important role in pathological processes of cerebral ischemia followed by reperfusion. The effect of 1, 5-dicaffeoylquinic acid (1, 5-diCQA) on primary culture rat cortical astrocytes induced by oxygen and glucose deprivation (OGD)/reperfusion was evaluated in this study. Appropriate concentration of 1, 5-diCQA pretreatment significantly suppressed cell death, reduced the production of reactive oxygen species, prevented glutathione (GSH) depletion, increased the activity of glutamate-cysteine ligase (GCL), and triggered Nrf2 nuclear translocation in astrocytes induced by 4 h of OGD and 20 h of reperfusion. Interestingly, these protective effects were greatly attenuated in Nrf2 siRNA-transfected cells. We conclude that 1, 5-diCQA has antioxidant signaling properties that upregulate GSH synthesis by stimulating the Nrf2 pathway in astrocytes and protects them from cell death in an in vitro model of ischemia/reperfusion. © 2010 Elsevier B.V. All rights reserved.

AB - Oxidative stress plays an important role in pathological processes of cerebral ischemia followed by reperfusion. The effect of 1, 5-dicaffeoylquinic acid (1, 5-diCQA) on primary culture rat cortical astrocytes induced by oxygen and glucose deprivation (OGD)/reperfusion was evaluated in this study. Appropriate concentration of 1, 5-diCQA pretreatment significantly suppressed cell death, reduced the production of reactive oxygen species, prevented glutathione (GSH) depletion, increased the activity of glutamate-cysteine ligase (GCL), and triggered Nrf2 nuclear translocation in astrocytes induced by 4 h of OGD and 20 h of reperfusion. Interestingly, these protective effects were greatly attenuated in Nrf2 siRNA-transfected cells. We conclude that 1, 5-diCQA has antioxidant signaling properties that upregulate GSH synthesis by stimulating the Nrf2 pathway in astrocytes and protects them from cell death in an in vitro model of ischemia/reperfusion. © 2010 Elsevier B.V. All rights reserved.

KW - 1,5-Dicaffeoylquinic acid

KW - Glutathione

KW - Ischemia/reperfusion

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ER -

1,5-Dicaffeoylquinic acid-mediated glutathione synthesis through activation of Nrf2 protects against OGD/reperfusion-induced oxidative stress in astrocytes

Abstract

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