miR-98-5p protects against cerebral ischemia/reperfusion injury through anti-apoptosis and anti-oxidative stress in mice

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]

Automated summary

miR-98-5p plays a protective role in cerebral ischemia/reperfusion injury by reducing infarction area, decreasing oxidative stress, and inhibiting apoptosis.