Acteoside Attenuates Oxidative Stress and Neuronal Apoptosis in Rats with Focal Cerebral Ischemia-Reperfusion Injury.

Abstract

Acteoside (ACT) has been shown to exert antioxidant and neuroprotective effects in neurodegenerative diseases. However, the effect of ACT on cerebral ischemia-reperfusion (I/R) injury is not yet clear. In this study, we found that ACT administration reduced infarct volume and brain edema, and improved neurological deficits, as indicated by the decreased modified neurological severity score. Administration of ACT strikingly reduced oxidative stress, accompanied by decreased levels of reactive oxygen species and malondialdehyde and increased levels of superoxide dismutase and catalase in a rat model of middle cerebral artery occlusion/reperfusion (MCAO/R). Furthermore, ACT administration reduced the number of terminal deoxynucleotidyl transferase uridine 5'-triphosphate (UTP) nick-end labeling-positive cells in the cerebral cortex of ischemic side of MCAO/R rats, accompanied by downregulation of B cell lymphoma 2 (Bcl-2) associated X protein and cleaved caspase-3 proteins and upregulation of Bcl-2 protein. Additionally, ACT treatment inhibited the protein kinase R/eukaryotic initiation factor-2α stress pathway in the brains of MCAO/R rats. Our results demonstrated that ACT attenuates oxidative stress and neuronal apoptosis in MCAO/R rats, suggesting that ACT may serve as a novel therapeutic candidate for the treatment of I/R brain injury.

• Authors: Dongjian Xia, Zhuang Zhang, Yuanli Zhao
• Journal: Biological & pharmaceutical bulletin (Biol Pharm Bull) Vol. 41 Issue 11 Pg. 1645-1651 ( 2018) ISSN: 1347-5215 [Electronic] Japan
• PMID: 30381663 (Publication Type: Journal Article)

Chemical References

• Antioxidants
• Glucosides
• Neuroprotective Agents
• Phenols
• Plant Extracts
• Proto-Oncogene Proteins c-bcl-2
• bcl-2-Associated X Protein
• acteoside
• Superoxide Dismutase
• Proto-Oncogene Proteins c-akt
• Caspase 3

Topics

• Animals
• Antioxidants (metabolism, pharmacology, therapeutic use)
• Apoptosis (drug effects)
• Brain (drug effects, metabolism, pathology)
• Brain Injuries (etiology, metabolism, pathology, prevention & control)
• Brain Ischemia (drug therapy, metabolism, pathology)
• Caspase 3 (metabolism)
• Glucosides (pharmacology, therapeutic use)
• Infarction, Middle Cerebral Artery
• Ischemia
• Magnoliopsida (chemistry)
• Male
• Neuroprotective Agents (pharmacology, therapeutic use)
• Oxidative Stress (drug effects)
• Phenols (pharmacology, therapeutic use)
• Phytotherapy
• Plant Extracts (pharmacology, therapeutic use)
• Proto-Oncogene Proteins c-akt (metabolism)
• Proto-Oncogene Proteins c-bcl-2 (metabolism)
• Rats, Wistar
• Reperfusion Injury (metabolism, pathology, prevention & control)
• Superoxide Dismutase
• Up-Regulation
• bcl-2-Associated X Protein