Hydroxysafflor Yellow A Shows Protection against PPARγ Inactivation in Nitrosative Neurons
Joint Authors
Sun, Li
Xu, Yan-Wei
Han, Jing
Xiao, Chen
Cao, Shan-Shan
Liang, Hao
Cheng, Yan
Source
Oxidative Medicine and Cellular Longevity
Issue
Vol. 2018, Issue 2018 (31 Dec. 2018), pp.1-13, 13 p.
Publisher
Hindawi Publishing Corporation
Publication Date
2018-10-16
Country of Publication
Egypt
No. of Pages
13
Main Subjects
Abstract EN
Peroxynitrite-mediated nitrosative stress in the brain has been associated with various neurodegenerative disorders.
Recent evidence highlights peroxisome proliferator-activated receptor γ (PPARγ) as a critical neuroprotective factor in neurodegenerative diseases.
Here, we observed the effect of the herb hydroxysafflor yellow A (HSYA) during nitrosative stress in neurons and investigated the mechanism based on PPARγ protection.
We found that a single exposure of primary neurons to peroxynitrite donor SIN-1 caused neuronal injury, which was accompanied by the increase of PPARγ nitration status and lack of activation of the receptor, as measured by PPARγ DNA-binding activity, by agonist (15d-PGJ2 or rosiglitazone) stimulation.
The crucial role of PPARγ in neuronal defense against nitrosative stress was verified by showing that pretreatment with 15d-PGJ2 or rosiglitazone attenuated SIN-1-induced neuronal injury but pretreatment with GW9662, a PPARγ antagonist, aggravated SIN-1-induced neuronal injury.
The addition of HSYA not only inhibited SIN-1-induced neuronal damage but prevented PPARγ nitrative modification and resumed PPARγ activity stimulated by either 15d-PGJ2 or rosiglitazone.
Furthermore, HSYA also showed the ability to rescue the neuroprotective effect of 15d-PGJ2 or rosiglitazone when the agonists were coincubated with SIN-1.
Finally, in vivo experiments demonstrated that the administration of HSYA also efficiently blocked PPARγ nitration and loss of activity in the SIN-1-injected hippocampus and reversed the increased neuronal susceptibility which was supported by the inhibition of Bcl-2 protein downregulation induced by SIN-1.
The results suggest that HSYA protects neurons from nitrosative stress through keeping PPARγ as a functional receptor, allowing a more effective activation of this neuroprotective factor by the endogenous or exogenous agonist.
Our findings provide new clues in understanding the role of the neuroprotective potential of the herbal HSYA.
American Psychological Association (APA)
Sun, Li& Xu, Yan-Wei& Han, Jing& Xiao, Chen& Cao, Shan-Shan& Liang, Hao…[et al.]. 2018. Hydroxysafflor Yellow A Shows Protection against PPARγ Inactivation in Nitrosative Neurons. Oxidative Medicine and Cellular Longevity،Vol. 2018, no. 2018, pp.1-13.
https://search.emarefa.net/detail/BIM-1212351
Modern Language Association (MLA)
Sun, Li…[et al.]. Hydroxysafflor Yellow A Shows Protection against PPARγ Inactivation in Nitrosative Neurons. Oxidative Medicine and Cellular Longevity No. 2018 (2018), pp.1-13.
https://search.emarefa.net/detail/BIM-1212351
American Medical Association (AMA)
Sun, Li& Xu, Yan-Wei& Han, Jing& Xiao, Chen& Cao, Shan-Shan& Liang, Hao…[et al.]. Hydroxysafflor Yellow A Shows Protection against PPARγ Inactivation in Nitrosative Neurons. Oxidative Medicine and Cellular Longevity. 2018. Vol. 2018, no. 2018, pp.1-13.
https://search.emarefa.net/detail/BIM-1212351
Data Type
Journal Articles
Language
English
Notes
Includes bibliographical references
Record ID
BIM-1212351