Journal
JOURNAL OF BIOCHEMISTRY
Volume 169, Issue 2, Pages 195-206Publisher
OXFORD UNIV PRESS
DOI: 10.1093/jb/mvaa099
Keywords
apoptosis; cerebral ischemia/reperfusion; mice; miR-98-5p; oxidative stress
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miR-98-5p plays a protective role in cerebral ischemia/reperfusion injury by reducing infarction area, decreasing oxidative stress, and inhibiting apoptosis.
Cerebral ischemia/reperfusion (I/R) injury is an obstacle in treating ischemic stroke effectively. miR-98-5p has been reported to have the ability of reducing myocardial I/R injury. To explore the function of miR-98-5p in cerebral I/R, we established mice model of middle cerebral artery occlusion and reperfusion (MCAO/R). The level of miR-98-5p was found to be downregulated in serum of stroke patients and brain tissues of MCAO/R mice. Examination of brain tissues indicated that upregulating miR-98-5p level alleviated the infarction in MCAO/R mice. Moreover, the upregulation of miR-98-5p reduced reactive oxygen species production and enhanced superoxide dismutase activity in brain tissues of MCAO/R mice. These results indicating that miR-98-5p could protect against oxidative stress. Further study showed that miR-98-5p inhibited apoptosis by reducing the levels of death-associated protein kinase 1, B cell lymphoma/leukaemia-2 associated x protein and cleaved caspase-3, as well as increasing the level of B cell lymphoma/leukaemia-2. In addition, miR-98-5p was found to protect against oxidative stress through downregulating the level of BTB domain and CNC homology 1 and upregulating the levels of NAD(P) H: quinone oxidoreductase 1 and heme oxygenase 1. Therefore, miR-98-5p might be a potential target to treat cerebral I/R injury. [GRAPHICS]
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