Oxymatrine protects rat brains against permanent focal ischemia and downregulates NF-κB expression

Liu, Ying; Zhang, Xiangjian; Yang, Chenhui; Fan, Huishou

doi:10.1016/j.brainres.2009.02.069

Cited by 85 publications

(48 citation statements)

References 23 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…27,34) The present study also demonstrated the efficacy of oxymatrine in CI/R, with significantly reduced neurological deficit scores, infarct volume and brain edema in OMT group at different times after operation, which is consistent with the effect of oxymatrine on Nrf2/HO-1 pathway. Furthermore, the degree of lipid peroxidation was also decreased by oxymatrine, directly suggesting a notably antioxidative action of oxymatrine during CI/R.…”

Section: Discussionsupporting

confidence: 87%

The Neuroprotection of Oxymatrine in Cerebral Ischemia/Reperfusion Is Related to Nuclear Factor Erythroid 2-Related Factor 2 (Nrf2)-Mediated Antioxidant Response: Role of Nrf2 and Hemeoxygenase-1 Expression

Zhang

Cui

et al. 2011

Biological & Pharmaceutical Bulletin

View full text Add to dashboard Cite

Cerebrovascular disease, a kind of common and frequently-occurring disease endangering the human health seriously, is one of the leading causes of death and disability worldwide, with the most frequent prevalence of ischemic cerebrovascular disease.1) Recanalization following ischemia is the most effective method for treatment of acute cerebral infarct and correction of hypoxia, but paradoxically causing severe cerebral ischemia-reperfusion (CI/R) injury. 2,3) Due to the lack of efficient neuroprotective therapies, the CI/R injury is still a major medical problem urgently needed to be further studied and discussed.A variety of cascade reactions induced by CI/R involve disequilibrium of calcium homeostasis, cytotoxicity of excitatory amino acid, oxidative stress, mitochondrial dysfunction, etc., [4][5][6] which has been accompanied by proteaseactivation and changing expression of genes, and ultimately resulting in neuron death and apoptosis. Increasing evidences suggest a critical role for oxidative stress in mediating tissue injury and neuron death during CI/R. 7,8) Brain is the most activated organ with aerobic metabolism, and produces a certain level of reactive oxygen species physiologically by aerobic metabolism, with a dynamic equilibrium of reactive oxygen species generation and elimination. Pathological unbalance occurs as the free radicals are produced excessively or endogenous anti-oxidative systems perform functional disturbance, and then, excessive accumulation of free radicals may induce oxidative reactions in attacked cells and tissues.9)The ability of free radicals production is greater than that of elimination by endogenous anti-oxidative systems in ischemic tissues especially in tissues after CI/R. 10) Elevated reactive oxygen species produced in cerebral ischemia could directly disrupt the structures of lipids, proteins and DNA, and induce cell death in various ways.11) Previous studies have well documented that increasing the activities of antioxidant enzymes, or administration of antioxidants, attenuates neuron damage during CI/R injury. [12][13][14] Conversely, lowering the antioxidant capacity increases neuron death after CI/R. 15)The nuclear factor erythroid 2-related factor 2 (Nrf2) pathway is a recently elucidated pathway to induce the production of antioxidant enzymes 16,17) -known as phase II enzymes including hemeoxygenase-1 (HO-1), reduced nicotinamide adenine dinucleotide phosphate (NADPH) quinone oxidoreductase 1, and g-glutamyl cysteine ligase (g-GCL)-through antioxidant-response element (ARE). Activating this way enhances the activities of those antioxidant enzymes and provides efficient cytoprotection, partly, by detoxifying reactive oxygen species and xenobiotics, regulating glutathione (GSH) production and use, and maintaining intracellular redox state. 18,19) Recent experiments have suggested that increasing the activity of Nrf2 and gene targets in cell culture models and stroke animal models that simulate components of cerebral ischemia damage is highly neuroprotective. 20,21...

show abstract

Section: Discussionsupporting

confidence: 87%

The Neuroprotection of Oxymatrine in Cerebral Ischemia/Reperfusion Is Related to Nuclear Factor Erythroid 2-Related Factor 2 (Nrf2)-Mediated Antioxidant Response: Role of Nrf2 and Hemeoxygenase-1 Expression

Zhang

Cui

et al. 2011

Biological & Pharmaceutical Bulletin

View full text Add to dashboard Cite

show abstract

“…OMT has been proved to have a variety of biological effects in treatment of viral hepatitis 8 , bronchial asthma 9 and ischemic injuries [10][11][12][13][14][15][16]22 , and plays a role in scavenging activity against reactive oxygen species 18 . In view of these considerations, we tested the therapeutic potentials of OMT on renal I/R injury rat model.…”

Section: Discussionmentioning

confidence: 99%

“…, liver 12 , intestinal 13 and brain [14][15][16] ischemia/reperfusion injury in animal models. OMT also have a protective role in adriamycin-induced chronic renal fibrosis 17 .…”

mentioning

confidence: 99%

Oxymatrine ameliorates renal ischemia-reperfusion injury from oxidative stress through Nrf2/HO-1 pathway

et al. 2015

View full text Add to dashboard Cite

PURPOSE:To investigate if oxymatrine pretreatment could ameliorate renal I/R injury induced in rats and explore the possible role of oxymatrine in Nrf2/HO-1 pathway. METHODS:Unilaterally nephrectomized rats were insulted by I/R in their left kidney. Twenty four rats were randomly divided into three groups: sham group, I/R + saline-treated group, I/R + OMT-treated group. Oxymatrine or vehicle solution was administered intraperitoneally injected 60 min before renal ischemia, respectively. Renal function, histology, makers of oxidative stress, cell apoptosis and Nrf2/HO-1 expressions were assessed. RESULTS:Oxymatrine pretreatment exhibited an improved renal functional recovery, alleviated histological injury and oxidative stress, inhibiting tubular apoptosis, and accompanied by upregulated the expression of Nrf2/HO-1 proteins. CONCLUSION:Oxymatrine may attenuate renal ischemia/reperfusion injury, and this renoprotective effect may be through activating the Nrf2/HO-1 pathway.

show abstract

“…Recently, it was reported that OMT could inhibit inflammatory brain injury, weaken cerebral edema, and provide neuroprotection against subsequent cerebral ischemic injury [14][15][16]. However, there have been few reports on the influence of OMT on TBI.…”

Section: Introductionmentioning

confidence: 99%

Oxymatrine reduces neuronal cell apoptosis by inhibiting Toll-like receptor 4/nuclear factor kappa-B-dependent inflammatory responses in traumatic rat brain injury

Dong

et al. 2010

Inflamm. Res.

View full text Add to dashboard Cite

show abstract

Oxymatrine protects rat brains against permanent focal ischemia and downregulates NF-κB expression

Cited by 85 publications

References 23 publications

The Neuroprotection of Oxymatrine in Cerebral Ischemia/Reperfusion Is Related to Nuclear Factor Erythroid 2-Related Factor 2 (Nrf2)-Mediated Antioxidant Response: Role of Nrf2 and Hemeoxygenase-1 Expression

The Neuroprotection of Oxymatrine in Cerebral Ischemia/Reperfusion Is Related to Nuclear Factor Erythroid 2-Related Factor 2 (Nrf2)-Mediated Antioxidant Response: Role of Nrf2 and Hemeoxygenase-1 Expression

Oxymatrine ameliorates renal ischemia-reperfusion injury from oxidative stress through Nrf2/HO-1 pathway

Oxymatrine reduces neuronal cell apoptosis by inhibiting Toll-like receptor 4/nuclear factor kappa-B-dependent inflammatory responses in traumatic rat brain injury

Contact Info

Product

Resources

About