Intracerebral Hemorrhage, Oxidative Stress, and Antioxidant Therapy

Duan, Xuanchu; Wen, Zunjia; Shen, Haitao; Shen, Meifen; Chen, Gang

doi:10.1155/2016/1203285

Cited by 239 publications

(188 citation statements)

References 197 publications

(206 reference statements)

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“…Accumulating evidence has demonstrated that oxidative stress plays an important role in the development of EBI (Ayer and Zhang, 2008; Duan et al, 2016). Following insults like hypoxia-ischemic or SAH, the production of reactive oxygen species (ROS) exceeds the ability of the endogenous anti-oxidant system, leading to oxidative stress and cell death (Wu et al, 2014; Zhang et al, 2016).…”

Section: Discussionmentioning

confidence: 99%

Neuroprotective Effects of a Smoothened Receptor Agonist against Early Brain Injury after Experimental Subarachnoid Hemorrhage in Rats

Hu¹,

Wang

et al. 2017

Front. Cell. Neurosci.

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The sonic hedgehog (Shh) signaling pathway plays a fundamental role in the central nervous system (CNS) development, but its effects on neural cell survival and brain repair after subarachnoid hemorrhage (SAH) has not been well-investigated. The present study was undertaken to evaluate the influence of an agonist of the Shh co-receptor Smoothened (Smo), purmorphamine (PUR), on early brain injury (EBI) as well as the underlying mechanisms after SAH. PUR was administered via an intraperitoneal injection with a dose of 0.5, 1, and 5 mg/kg at 2, 6, 24, and 46 h after SAH in rat model. The results showed that PUR treatment significantly ameliorated brain edema, improved neurobehavioral function, and attenuated neuronal cell death in the prefrontal cortex (PFC), associated with a decrease in Bax/Bcl-2 ratio and suppression of caspase-3 activation at 48 h after SAH. PUR also promoted phospho-ERK levels. Additionally, PUR treatment markedly decreased MDA concentration accompanied with the elevation in the expression of nuclear factor erythroid 2-related factor 2 and heme oxygenase-1 in PFC. Notably, PUR treatment significantly reversed the changes of Shh pathway mediators containing Patched, Gli1, and Shh by SAH insult, and the neuroprotection of PUR on SAH was blocked by Smo antagonist cyclopamine. These results indicated that PUR exerts neuroprotection against SAH-evoked injury in rats, mediated in part by anti-apoptotic and anti-oxidant mechanism, up-regulating phospho-ERK levels, mediating Shh signaling molecules in the PFC.

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Section: Discussionmentioning

confidence: 99%

Neuroprotective Effects of a Smoothened Receptor Agonist against Early Brain Injury after Experimental Subarachnoid Hemorrhage in Rats

Hu¹,

Wang

et al. 2017

Front. Cell. Neurosci.

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“…Inflammatory reaction and cell apoptosis importance has increased in the ICH process, which leads to cerebral edema and secondary brain injury 21,22. Activation of neutrophils, macrophages and microglia enhances secretion large amount of inflammatory factors, such as TNF-α, IL-1β, IL-6 and IL-8, etc.…”

Section: Discussionmentioning

confidence: 99%

The role of heme oxygenase-1 (HO-1) in the regulation of inflammatory reaction, neuronal cell proliferation and apoptosis in rats after intracerebral hemorrhage (ICH)

Xue-zheng¹,

2016

NDT

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ObjectiveTo investigate the role of heme oxygenase-1 (HO-1) in the regulation of inflammatory reaction, neuronal cell proliferation and apoptosis in rats after intracerebral hemorrhage (ICH).MethodsThirty-six adult Sprague Dawley (SD) male rats were randomly divided into sham operation, ICH and zinc protoporphyrin (ZPP) group. Rats (except for the sham operation group) were given 50 μL stereotactic injection of autologous blood from the femoral artery into the caudate nucleus, to establish an ICH model. In addition, rats in the ZPP group were given 10 mg/kg intraperitoneal injection of ZPP. At day 3 postoperative, neurobehavioral changes and brain water content were evaluated, brain tissue HO-1 expression was detected with immunohistochemistry and reverse transcription polymerase chain reaction (RT-PCR), brain tissue apoptosis was evaluated with TUNEL method, Caspase 3, Caspase 8 and Caspase 9 activity were detected with colorimetric method, level of TNF-α, IL-1β, IL-6 and IL-8 were measured with the enzyme-linked immunosorbent assay (ELISA), while Bcl-2, Bax, p-NF-κB p65 and p-IκBα protein expression were detected with Western blot.ResultsICH group compared to sham operation: HO-1 positive rate and mRNA expression were increased, neurological deficit score and cell apoptosis rate were increased, Caspase 3, Caspase 8 and Caspase 9 activity were increased, level of TNF-α, IL-1β, IL-6 and IL-8 were increased, Bcl-2 expression was downregulated, Bax, p-NF-κB p65 and p-IκBα expression were upregulated. The differences were statistically significant (P<0.01). ZPP group compared to ICH: HO-1 positive rate and mRNA expression were decreased, neurological deficit score and cell apoptosis rate were decreased, Caspase 3, Caspase 8, Caspase 9 activity were decreased, level of TNF-α, IL-1β, IL-6 and IL-8 were decreased, Bcl-2 expression was upregulated, Bax, p-NF-κB p65 and p-IκBα expression were downregulated, and the differences were statistically significant (P<0.01).ConclusionHO-1 inhibitor, ZPP does have a protective effect on ICH rats. This might be due to its inhibition to the inflammatory reaction and neuronal cell apoptosis.

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“…In 1996, CBS activation named S-adenylyl methionine was revealed which efficiently decreased in individuals with AD [31] because when endogenous level of H 2 S decreases, it causes accretion of homocysteine level in the brain eventually [151]. Many studies including in vitro and in vivo studies shows that H 2 S has a prominent role in cell growth promotion and preservation of the function of the factors like amyloid beta (A β ) peptides, malondialdehyde (MDA), hypochlorite (HOCL), and 4-hydroxy-2-nonenal (4-HNE) which causes oxidative stress [15, 152]. In a study of adult male Wister rats, null H 2 S toxicity has the capacity to increase cognition by lowering A β plaques and triggering the APP, PST, and ON/4R-tau isoforms.…”

Section: Oxidative Stress and Gasotransmittersmentioning

confidence: 99%

Role of Gasotransmitters in Oxidative Stresses, Neuroinflammation, and Neuronal Repair

Shefa

Yeo

Kim

et al. 2017

BioMed Research International

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To date, three main gasotransmitters, that is, hydrogen sulfide (H2S), carbon monoxide (CO), and nitric oxide (NO), have been discovered to play major bodily physiological roles. These gasotransmitters have multiple functional roles in the body including physiologic and pathologic functions with respect to the cellular or tissue quantities of these gases. Gasotransmitters were originally known to have only detrimental and noxious effects in the body but that notion has much changed with years; vast studies demonstrated that these gasotransmitters are precisely involved in the normal physiological functioning of the body. From neuromodulation, oxidative stress subjugation, and cardiovascular tone regulation to immunomodulation, these gases perform critical roles, which, should they deviate from the norm, can trigger the genesis of a number of neurodegenerative diseases such as Alzheimer's disease (AD) and Parkinson's disease (PD). The purpose of this review is to discuss at great length physical and chemical properties and physiological actions of H2S, NO, and CO as well as shedding light on recently researched molecular targets. We particularly put emphasis on the roles in neuronal inflammation and neurodegeneration and neuronal repair.

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Intracerebral Hemorrhage, Oxidative Stress, and Antioxidant Therapy

Cited by 239 publications

References 197 publications

Neuroprotective Effects of a Smoothened Receptor Agonist against Early Brain Injury after Experimental Subarachnoid Hemorrhage in Rats

Neuroprotective Effects of a Smoothened Receptor Agonist against Early Brain Injury after Experimental Subarachnoid Hemorrhage in Rats

The role of heme oxygenase-1 (HO-1) in the regulation of inflammatory reaction, neuronal cell proliferation and apoptosis in rats after intracerebral hemorrhage (ICH)

Role of Gasotransmitters in Oxidative Stresses, Neuroinflammation, and Neuronal Repair

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