Astaxanthin Activates Nuclear Factor Erythroid-Related Factor 2 and the Antioxidant Responsive Element (Nrf2-ARE) Pathway in the Brain after Subarachnoid Hemorrhage in Rats and Attenuates Early Brain Injury

Autor: Meng-Liang Zhou, Xiaoliang Wang, Qi Wu, Wei Li, Xin Zhang, Xiang-Sheng Zhang, Handong Wang, Qing Yu
Rok vydání: 2014
Předmět:
Male
Pathology
Antioxidant
medicine.medical_treatment
Pharmaceutical Science
Apoptosis
Xanthophylls
Pharmacology
medicine.disease_cause
Antioxidants
Rats
Sprague-Dawley
nuclear factor erythroid-related factor 2
chemistry.chemical_compound
early brain injury
Drug Discovery
NAD(P)H Dehydrogenase (Quinone)
lcsh:QH301-705.5
Pharmacology
Toxicology and Pharmaceutics (miscellaneous)
Glutathione Transferase
medicine.diagnostic_test
Brain
Isoenzymes
astaxanthin
Blood-Brain Barrier
Immunohistochemistry
Signal Transduction
medicine.medical_specialty
Subarachnoid hemorrhage
NF-E2-Related Factor 2
subarachnoid hemorrhage
Article
Western blot
medicine
Animals
cardiovascular diseases
business.industry
Glutathione
medicine.disease
Antioxidant Response Elements
Rats
nervous system diseases
Disease Models
Animal
Oxidative Stress
lcsh:Biology (General)
chemistry
Brain Injuries
NAD+ kinase
business
Heme Oxygenase-1
Oxidative stress
Zdroj: Marine Drugs, Vol 12, Iss 12, Pp 6125-6141 (2014)
Marine Drugs
Volume 12
Issue 12
Pages 6125-6141
ISSN: 1660-3397
Popis: Astaxanthin (ATX) has been proven to ameliorate early brain injury (EBI) after experimental subarachnoid hemorrhage (SAH) by modulating cerebral oxidative stress. This study was performed to assess the effect of ATX on the Nrf2-ARE pathway and to explore the underlying molecular mechanisms of antioxidant properties of ATX in EBI after SAH. A total of 96 male SD rats were randomly divided into four groups. Autologous blood was injected into the prechiasmatic cistern of the rat to induce an experimental SAH model. Rats in each group were sacrificed at 24 h after SAH. Expressions of Nrf2 and heme oxygenase-1 (HO-1) were measured by Western blot and immunohistochemistry analysis. The mRNA levels of HO-1, NAD (P) H: quinone oxidoreductase 1 (NQO-1), and glutathione S-transferase-α1 (GST-α1) were determined by real-time polymerase chain reaction (PCR). It was observed that administration of ATX post-SAH could up-regulate the cortical expression of these agents, mediated in the Nrf2-ARE pathway at both pretranscriptional and posttranscriptional levels. Meanwhile, oxidative damage was reduced. Furthermore, ATX treatment significantly attenuated brain edema, blood–brain barrier (BBB) disruption, cellular apoptosis, and neurological dysfunction in SAH models. This study demonstrated that ATX treatment alleviated EBI in SAH model, possibly through activating the Nrf2-ARE pathway by inducing antioxidant and detoxifying enzymes.
Databáze: OpenAIRE
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