Activation of the Nrf2 defense pathway contributes to neuroprotective effects of phloretin on oxidative stress injury after cerebral ischemia/reperfusion in rats

2015 ◽  
Vol 351 (1-2) ◽  
pp. 88-92 ◽  
Author(s):  
Yu Liu ◽  
Lei Zhang ◽  
Jiangjiu Liang
Keyword(s):  
Oxidative Stress ◽  
Cerebral Ischemia ◽  
Ischemia Reperfusion ◽  
Neuroprotective Effects ◽  
Stress Injury ◽  
Cerebral Ischemia Reperfusion ◽  
Oxidative Stress Injury

scholarly journals Metformin Protects against Oxidative Stress Injury Induced by Ischemia/Reperfusion via Regulation of the lncRNA-H19/miR-148a-3p/Rock2 Axis

2019 ◽  
Vol 2019 ◽  
pp. 1-18 ◽  
Author(s):  
Jing Zeng ◽  
Long Zhu ◽  
Jing Liu ◽  
Tao Zhu ◽  
Zhaohui Xie ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Ischemic Stroke ◽  
Cerebral Ischemia ◽  
Ischemia Reperfusion ◽  
Luciferase Reporter ◽  
Neuroprotective Effects ◽  
Stress Injury ◽  
Oxidative Stress Injury

Previous studies have shown that metformin not only is a hypoglycemic agent but also has neuroprotective effects. However, the mechanism of action of metformin in ischemic stroke is unclear. Oxidative stress is an important factor in the pathogenesis of cerebral ischemia-reperfusion injury. It has been reported that metformin is associated with stroke risk in the clinical population. This study is aimed at investigating the effect and mechanism of metformin in an experimental model of oxidative stress induced by ischemia/reperfusion (I/R) in vivo and oxygen glucose deprivation/reperfusion (OGD/R) in vitro. Metformin (100, 200, and 300 mg/kg) was administered intraperitoneally immediately after induction of cerebral ischemia. The indicators of oxidative stress selected were antioxidant enzyme activities of catalase, malondialdehyde (MDA), nitric oxide (NO), superoxide dismutase (SOD), and glutathione peroxidation enzyme (GSHPx). First, we demonstrated that metformin can significantly alleviate acute and chronic cerebral I/R injury and it has a strong regulatory effect on stroke-induced oxidative stress. It can reduce the elevated activities of MDA and NO and increase the levels of GSHPx and SOD in the cerebrum of mice and N2a cells exposed to I/R. Furthermore, real-time PCR and western blot were used to detect the expression of long noncoding RNA H19 (lncRNA-H19), microRNA-148a-3p (miR-148a-3p), and Rho-associated protein kinase 2 (Rock2). The direct interaction of lncRNA-H19, miR-148a-3p, and Rock2 was tested using a dual luciferase reporter assay. lncRNA-H19 altered OGD/R-induced oxidative stress by modulating miR-148a-3p to increase Rock2 expression. The expression of lncRNA-H19 and Rock2 could be downregulated with metformin in vivo and in vitro. In conclusion, our study confirmed that metformin exerts neuroprotective effects by regulating ischemic stroke-induced oxidative stress injury via the lncRNA-H19/miR-148a-3p/Rock2 axis. These results provide new evidence that metformin may represent a potential treatment for stroke-related brain injury.

Carvacryl acetate, a semisynthetic monoterpenic ester obtained from essential oils, provides neuroprotection against cerebral ischemia reperfusion-induced oxidative stress injury via the Nrf2 signalling pathway

2020 ◽  
Vol 11 (2) ◽  
pp. 1754-1763
Author(s):  
Ying Song ◽  
Li-Bo Wang ◽  
Yun Bei ◽  
Dong-Xu Qin ◽  
Li-Yao Ai ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cerebral Ischemia ◽  
Essential Oils ◽  
Ischemia Reperfusion ◽  
Signalling Pathway ◽  
Stress Injury ◽  
Cerebral Ischemia Reperfusion ◽  
Oxidative Stress Injury

Carvacryl acetate (CA) is a semisynthetic monoterpenic ester obtained from essential oils, and it exerts an antioxidation effect.

MicroRNA-23a-3p attenuates oxidative stress injury in a mouse model of focal cerebral ischemia-reperfusion

2014 ◽  
Vol 1592 ◽  
pp. 65-72 ◽  
Author(s):  
Haiping Zhao ◽  
Zhen Tao ◽  
Rongliang Wang ◽  
Ping Liu ◽  
Feng Yan ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cerebral Ischemia ◽  
Mouse Model ◽  
Focal Cerebral Ischemia ◽  
Ischemia Reperfusion ◽  
Stress Injury ◽  
Cerebral Ischemia Reperfusion ◽  
Oxidative Stress Injury

scholarly journals Low expression of miR‑532‑3p contributes to cerebral ischemia/reperfusion oxidative stress injury by directly targeting NOX2

2020 ◽  
Vol 22 (3) ◽  
pp. 2415-2423
Author(s):  
Li Mao ◽  
Mei‑Ling Zuo ◽  
Ai‑Ping Wang ◽  
Ying Tian ◽  
Li‑Chen Dong ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cerebral Ischemia ◽  
Ischemia Reperfusion ◽  
Stress Injury ◽  
Cerebral Ischemia Reperfusion ◽  
Oxidative Stress Injury ◽  
Low Expression

scholarly journals Effects of Alpha-Mangostin Encapsulated in Nanostructured Lipid Carriers in Mice with Cerebral Ischemia Reperfusion Injury

2021 ◽  
Vol 50 (7) ◽  
pp. 2007-2015
Author(s):  
Romgase Sakamula ◽  
Teerapong Yata ◽  
Wachiryah Thong-asa
Keyword(s):  
Oxidative Stress ◽  
Cerebral Ischemia ◽  
Cerebral Infarction ◽  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Nanostructured Lipid Carriers ◽  
Neuroprotective Effects ◽  
Cerebral Ischemia Reperfusion ◽  
Cerebral Ischemia Reperfusion Injury

Cerebral ischemia reperfusion injury (CIRI) is a phenomenon in which the cerebral blood supply is restored after a period of ischemia, resulting in irreversible damage to brain tissue. Oxidative stress plays a crucial role in the development of CIRI, therefore, targeting oxidative stress might be an effective strategy for CIRI prevention and treatment. Many therapeutic substances possess antioxidant and protective properties against neurodegenerative disorders but lack of in vivo application due to their solubility, and bioavailability. We investigated the effects of alpha-mangostin (αM) encapsulated in nanostructured lipid carriers (αM-NLC) on CIRI in mice. Forty male ICR mice were randomly divided into four groups: Sham, ischemia reperfusion (IR), ischemia reperfusion with 25 mg/kg of αM (IR+αM), and ischemia reperfusion with 25 mg/kg of αM-NLC (IR+αM-NLC). After 6 days of oral administrations, IR was delivered using 30 min of bilateral common carotid artery occlusion, followed by 45 min of reperfusion. Cerebral infarction volume, hippocampal neuronal and corpus callosum (CC) white matter damage, malondialdehyde (MDA) level, and catalase (CAT) activity were evaluated. Our results indicated that αM and αM-NLC prevent lipid peroxidation as well as hippocampal CA1, CA3, and CC damage (p<0.05). Only αM-NLC prevented cerebral infarction and enhanced CAT activity (p<0.05). We therefore conclude that αM and αM-NLC have neuroprotective effects against CIRI, and NLC increases therapeutic efficacy of αM against CIRI.

scholarly journals Scutellarin acts on the AR-NOX Axis to Remediate Oxidative Stress Injury in a Mouse Model of Cerebral Ischemia/Reperfusion Injury

2021 ◽  
Author(s):  
Llin Peng ◽  
Minzhen Deng ◽  
Yan Huang ◽  
Shuang Wu ◽  
Yucheng Cao ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Ischemic Stroke ◽  
Cerebral Ischemia ◽  
Brain Damage ◽  
Ischemia Reperfusion ◽  
Ischemic Injury ◽  
Neurological Function ◽  
Enzyme Linked Immunosorbent Assay ◽  
Stress Injury ◽  
Oxidative Stress Injury

Abstract BackbroundOxidative stress plays an important role in the ischemic stroke induced brain damage. Our previous study showed that Scutellarin protects against ischemic injury in vitro and in vivo induced oxidative damage in rats, and we also reported that the involvement of Aldose reductase (AR) in oxidative stress and cerebral ischemic injury, in this study we furtherly explicit whether the antioxidant effect of Scutellarin on cerebral ischemia injury is related to AR gene regulation and its specific mechanism.MethodsC57BL/6N mice (Wild-type, WT) and AR knockout (AR-/-) mice were subjected to transient middle cerebral artery occlusion (tMCAO) model with 1h occlusion followed by 3d reperfusion, and Scutellarin was administered from 2h before surgery to 3 days after surgery. Subsequently, Neurological function were assessed by the modified Longa score method, the histopathological morphology observed with 2,3,5-triphenyltetrazolium chloride and hematoxylin-eosin staining. Enzyme-linked immunosorbent assay was used to detect the levels of ROS, 4-hydroxynonenal (4-HNE), 8-hydroxydeoxyguanosine (8-OHDG), Neurotrophin-3 (NT-3), poly ADP-ribose polymerase-1 (PARP1) and 3-nitrotyrosine (3-NT) in the ischemic penumbra regions. Quantitative proteomics profiling using quantitative nano-HPLC-MS/MS were performed to compare the protein expression difference between AR-/- and WT mice with or without tMCAO injury. The expression of AR, NOX1, NOX2 and NOX4 in the ipsilateral side of ischemic brain were detected by Real time-PCR, Western blot and immunofluorescence co-staining with NeuN.ResultsScutellarin treatment alleviated brain damage suffered from tMCAO injury such as improved neurological function deficit, brain infarct area and neuronal injury and reduced the expression of oxidation-related products, moreover, also down-regulated tMCAO induced AR mRNA and protein expression.ConclusionsScutellarin would be a potential drug for the treatment of ischemic stroke through regulating AR-NOX Axis modulate oxidative stress injury to play the protective role of cerebral ischemia injury.

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