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)

Danhong injection, a Chinese Materia Medica standardized product extracted from Radix Salviae miltiorrhizae and Flos Carthami tinctorii, is used extensively for the treatment of cerebrovascular diseases such as acutely cerebral infarction in clinic. In this study, we further investigated the mechanisms of Danhong injection on cerebral ischemia/reperfusion (I/R) damage relating to Nrf2/ARE signalling pathway in vivo and in vitro. For in vivo experiment, cerebral I/R injury was induced through middle cerebral artery occlusion. Rats were randomly divided into five groups: sham-operated group, I/R injury group, 6 mg/kg edaravone injection (positive control drug) group, 0.9 ml/kg Danhong injection (DHI-L) group, 1.8 ml/kg Danhong injection (DHI-H) group. The neurological score, cerebral infarction and brain edema were assessed while levels of superoxide dismutase (SOD), glutathione (GSH) and malondialdehyde (MDA) in brain tissue were also evaluated. Transcription levels of nuclear factor erythroid 2-related factor 2 (Nrf2), heme oxygenase-1 (HO-1), NAD(P)H: quinone oxidoreductase 1 (NQO1) were analysed by real-time polymerase chain reaction. For in vitro experiment, mouse Neuro-2A cells were wounded with H2O2 then cell viability and mRNA transcriptions levels of Nrf2, HO-1, NQO1 were detected. Protein expression level of Nrf2 was assayed by western blotting. The results showed that Danhong injection could ameliorate neurological score, cerebral infarction and brain edema. Also it can increase levels of SOD, GSH and decrease of MDA and upregulate expressions of Nrf2, HO-1, NQO1 in ischemic brain tissue in vivo. What's more, it increased the mRNA transcription of Nrf2 and HO-1 and upregulated protein expression of Nrf2 in vitro. These findings suggested that Danhong injection could prevent I/R-induced brain damage through activating Nrf2/ARE signaling pathway.
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PMID:Danhong injection attenuates ischemia/reperfusion-induced brain damage which is associating with Nrf2 levels in vivo and in vitro. 2506 40

Oxidative damage plays a critical role in many diseases of the central nervous system. This study was conducted to determine the molecular mechanisms involved in the putative anti-oxidative effects of sevoflurane against experimental stroke. Focal cerebral ischemia was performed via 1h of middle cerebral artery occlusion followed by reperfusion. At the onset of reperfusion, rats were subjected to postconditioning with sevoflurane or without sevoflurane for 1h. Neurological deficit score was assessed at different time points after reperfusion. Cerebral infarct volume, oxidative stress level and the binding activity of Nrf2 to antioxidant response element were assessed, meanwhile the expression of nuclear factor-erythroid 2-related factor 2 (Nrf2), quinine oxidoreductase 1 (NQO1), protein kinase B (Akt) and phosphor-Akt was examined by Western blot at 72h after reperfusion. Sevoflurane postconditioning administration significantly reduced neurological deficit score, infarct volume and oxidative stress levels, while increased the expression of phosphorylation Akt, NQO1, Nrf2 and the binding activity of Nrf2 to ARE in middle cerebral artery occlusion rats. These neuroprotective effects were all suppressed by LY294002, a selective PI3K blocker. Taken together, these findings provided evidence that sevoflurane postconditioning protects brain against ischemic/reperfusion injury, and this neuroprotective effect involves the Akt/Nrf2 pathway.
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PMID:Sevoflurane postconditioning attenuates cerebral ischemia-reperfusion injury via protein kinase B/nuclear factor-erythroid 2-related factor 2 pathway activation. 2514 26

Cerebral ischemia/reperfusion (I/R) usually leads to the exacerbation of brain injury. In the present research, the effect of BTB and CNC homology 1 (BACH1) on cerebral I/R injury was studied. Mice model of middle cerebral artery occlusion/reperfusion (MCAO/R) and Neuro-2a (N2a) cell model of oxygen-glucose deprivation/reoxygenation (OGD/R) were established to investigate the role of BACH1. It was found that MCAO/R mice expressed much higher BACH1 in the brain tissues accompanied with severe cerebral infarction, whereas downregulation of BACH1 reduced the infarction in MCAO/R mice. TUNEL staining showed that the downregulation of BACH1 inhibited apoptosis in brain tissues of MCAO/R mice. The expression of cleaved caspase-3 and cleaved PARP were also decreased by the downregulation of BACH1. Reactive oxygen species (ROS) and 3-nitrotyrosine (3-NT) staining showed that the downregulation of BACH1 reduced the levels of ROS and 3-NT. Moreover, less malondialdehyde (MDA) and more superoxide dismutase (SOD), heme oxygenase-1 (HO-1) and NAD(P)H: quinone oxidoreductase 1 (NQO1) were detected in MCAO/R mice pretreated with BACH1 shRNA, indicating that the downregulation of BACH1 reduced the oxidative stress. Similar conclusions were obtained from the further studies on N2a cells of OGD/R. We found that the downregulation of BACH1 reduced cell damage, oxidative stress and apoptosis in N2a cells. It was also demonstrated that the downregulation of BACH1 functioned through HO-1 and NQO1, which played important roles in protecting against cerebral I/R injury. Thus, BACH1 might be a potential therapeutic target for preventing cerebral I/R injury.
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PMID:Downregulation of BACH1 Protects AGAINST Cerebral Ischemia/Reperfusion Injury through the Functions of HO-1 and NQO1. 3231 10