Osteopontin attenuates early brain injury through regulating autophagy‐apoptosis interaction after subarachnoid hemorrhage in rats

Aim To determine the effect of osteopontin (OPN) on autophagy and autophagy‐apoptosis interactions after SAH. Methods The endovascular perforation model of SAH or sham surgery was performed in a total of 86 Sprague‐Dawley male rats. The temporal expressions of endogenous OPN and autophagy‐related pr...

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Published in:CNS neuroscience & therapeutics 2019-10, Vol.25 (10), p.1162-1172
Main Authors: Sun, Cheng‐Mei, Enkhjargal, Budbazar, Reis, Cesar, Zhou, Ke‐Ren, Xie, Zhi‐Yi, Wu, Ling‐Yun, Zhang, Tong‐Yu, Zhu, Qi‐Quan, Tang, Ji‐Ping, Jiang, Xiao‐Dan, Zhang, John H.
Format: Article
Language:English
Subjects:
Administration, Intranasal
Aneurysms
Animals
Apoptosis
Apoptosis - drug effects
Apoptosis - physiology
Autophagy
Autophagy - drug effects
Autophagy - physiology
Bax protein
Brain Injuries - metabolism
Brain Injuries - pathology
Brain Injuries - prevention & control
Brain injury
Cardiovascular system
Caspase
early brain injury
Male
Neurological complications
Original
Osteopontin
Osteopontin - administration & dosage
Osteopontin - biosynthesis
Phagocytosis
Proteins
Random Allocation
Rats
Rats, Sprague-Dawley
Subarachnoid hemorrhage
Subarachnoid Hemorrhage - drug therapy
Subarachnoid Hemorrhage - metabolism
Subarachnoid Hemorrhage - pathology
Surgery
Traumatic brain injury
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Summary:Aim To determine the effect of osteopontin (OPN) on autophagy and autophagy‐apoptosis interactions after SAH. Methods The endovascular perforation model of SAH or sham surgery was performed in a total of 86 Sprague‐Dawley male rats. The temporal expressions of endogenous OPN and autophagy‐related proteins (Beclin 1, ATG5, LC3 II to I ratio) were measured in sham and SAH rats at different time points (3, 6, 12, 24, and 72 hours). Rats were randomly divided into three groups: Sham, SAH + Vehicle (PBS, phosphate‐buffered saline), and SAH + rOPN (5 μg/rat recombinant OPN). Neurobehavioral tests were performed 24 hours after SAH, followed by the collection of brain samples for assessment of autophagy and apoptosis proteins. These tests assessed whether an autophagy‐apoptosis relationship existed on the histological level in the brain. Results Endogenous OPN and autophagy‐related proteins all increased after SAH. rOPN administration improved neurological dysfunction, increased the expression of autophagy‐related proteins (Beclin 1, ATG5, LC3 II to I ratio) and antiapoptotic protein Bcl‐2, while decreasing the expression of proapoptotic proteins (cleaved Caspase‐3 and Bax). rOPN also regulated autophagy‐apoptosis interactions 24 hours after SAH. Conclusion rOPN attenuates early brain injury and inhibits neuronal apoptosis by activating autophagy and regulating autophagy‐apoptosis interactions.
ISSN:1755-5930
1755-5949
DOI:10.1111/cns.13199