Selective Adenosine A Receptor Inhibitor SCH58261 Reduces Oligodendrocyte Loss Upon Brain Injury in Young Rats

Overview

Journal Saudi J Biol Sci

Specialty Biology

Date 2021 Jan 11

PMID 33424311

Citations 4

Authors

Mohamed A Al-Griw

Rabia O Alghazeer

Nuri Awayn

Ghalia Shamlan

Areej A Eskandrani

Afnan M Alnajeebi

Nouf A Babteen

Wafa S Alansari

Affiliations

Soon will be listed here.

Abstract

Cellular elements of maturing brain are vulnerable to insults, which lead to neurodevelopmental defects. There are no established treatments at present. Here we examined the efficacy of selective adenosine A receptor inhibitor SCH58261 to combat brain injury, particularly oligodendrocyte (OL) lineage cells, in young rats. Wistar rats (n = 24, 6.5 days old) were randomly divided into equal groups of four. The sham (SHAM) group received no treatment, the vehicle (VEHICLE) group received 0.1% dimethylsufoxide, the injury (INJ) group was exposed to oxygen-glucose deprivation insult, and the injury+SCH58261 (INJ+SCH58261) group was exposed to the insult and received 1 μM SCH58261. Immunocytochemical experiments revealed that there was a significant reduction in the populations of mature OL (MBP OLs) and immature OL precursors (NG2 OPCs) in the INJ group compared to SHAM group. Furthermore, there was also a significant increase in the percent of apoptotic MBP OL and NG2 OPC populations as evidenced by TUNEL assay. In addition, there was a significant reduction in the proliferation rate among NG2 OPCs, which was confirmed by BrdU immunostaining. On the other hand, treatment with SCH58261 significantly enhanced survival, evidenced by the reduction in apoptotic indices for both cell types, and it is preserved the NG2 OPC proliferation. Activation of adenosine A receptors may contribute to OL lineage cell loss in association with decreased mitotic behavior of OPCs in neonatal brains upon injury. Future investigations assessing ability of SCH58261 to regenerate myelin will provide insights into its wider clinical relevance.

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