Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:1.6.5.2 (NQO1)
 6,196 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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 (ROS) production and enhanced superoxide dismutase (SOD) 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 (DAPK1), B cell lymphoma/leukmia-2 (Bcl-2) associated x protein (Bax) and cleaved caspase-3, as well as increasing the level of Bcl-2. In addition, miR-98-5p was found to protect against oxidative stress through downregulating the level of BTB domain and CNC homology 1 (BACH1) and upregulating the levels of NAD(P)H: quinone oxidoreductase 1 (NQO1) and heme oxygenase 1 (HO-1). Therefore, miR-98-5p might be a potential target to treat cerebral I/R injury.
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PMID:miR-98-5p Protects Against Cerebral ischemia/reperfusion Injury Through Anti-apoptosis and Anti-oxidative stress in Mice. 3285 43