Oxidative Stress and the Central Nervous System

Salim, Samina

doi:10.1124/jpet.116.237503

Cited by 965 publications

(599 citation statements)

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“…Oxidative stress and inflammation are supposed to be the main direct factors in the progress of many cerebral diseases, such as ischemic stroke, traumatic brain injury, Alzheimer's disease, and Parkinson's disease (Abdul‐Muneer, Chandra, & Haorah, ; Salim, ; Yin, Sancheti, Patil, & Cadenas, ; Zhang et al, ). Brain cells, with their high energy demand, rich lipid content, and weak antioxidant capacity, are particularly vulnerable to oxidative damage (Salim, ). To add insult to brain injury, inflammatory processes are being correlated with alterations in cellular metabolism (Yin et al, ).…”

Section: Discussionmentioning

confidence: 99%

Panax notoginseng saponins suppress lipopolysaccharide‐induced barrier disruption and monocyte adhesion on bEnd.3 cells via the opposite modulation of Nrf2 antioxidant and NF‐κB inflammatory pathways

Liu

et al. 2019

Phytotherapy Research

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Dysfunction of the blood‐brain barrier (BBB) is a prerequisite for the pathogenesis of many cerebral diseases. Oxidative stress and inflammation are well‐known factors accounting for BBB injury. Panax notoginseng saponins (PNS), a clinical commonly used drug against cerebrovascular disease, possess efficient antioxidant and anti‐inflammatory activity. In the present study, the protective effects of PNS on lipopolysaccharide (LPS)‐insulted cerebral microvascular endothelial cells (bEnd.3) were assessed and the underlying mechanisms were investigated. The results showed that PNS mitigated the decrease of Trans‐Endothelial Electrical Resistance, increase of paracellular permeability, and loss of tight junction proteins in bEnd.3 BBB model. Meanwhile, PNS suppressed the THP‐1 monocytes adhesion on bEnd.3 monolayer. Moreover, PNS prevented the pro‐inflammatory cytokines secretion and reactive oxygen species generation in bEnd.3 cells stimulated with LPS. Mechanism investigations suggested that PNS promoted the Akt phosphorylation, activated Nrf2 antioxidant signaling, and inhibited the NF‐κB activation. All the effects of PNS could be abolished by PI3K inhibition at different levels. Taken together, these observations suggest that PNS may act as an extrinsic regulator that activates Nrf2 antioxidant defense system depending on PI3K/Akt and inhibits NF‐κB inflammatory signaling to attenuate LPS‐induced BBB disruption and monocytes adhesion on cerebral endothelial cells in vitro.

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Section: Discussionmentioning

confidence: 99%

Panax notoginseng saponins suppress lipopolysaccharide‐induced barrier disruption and monocyte adhesion on bEnd.3 cells via the opposite modulation of Nrf2 antioxidant and NF‐κB inflammatory pathways

Liu

et al. 2019

Phytotherapy Research

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“…Nonetheless, the hypothesis that oxidative stress is involved in the genesis of anxiety has been widely proposed (Bouayed et al, 2009 and Hassan et al, 2014). The neurobiological mechanisms may involve brain regions such as the amygdala and the hippocampus, which are especially sensitive to oxidative damage (Masood et al, 2008, Salim, 2016 and Salim et al, 2010) and which are implicated in anxiety-related disorders (Shin and Liberzon, 2010). Oxidative stress may lead to neuroendocrine alterations in the amygdala, including dendritic shrinkage and amygdala hyperactivity (Salim, 2016).…”

Section: Discussionmentioning

confidence: 99%

“…The neurobiological mechanisms may involve brain regions such as the amygdala and the hippocampus, which are especially sensitive to oxidative damage (Masood et al, 2008, Salim, 2016 and Salim et al, 2010) and which are implicated in anxiety-related disorders (Shin and Liberzon, 2010). Oxidative stress may lead to neuroendocrine alterations in the amygdala, including dendritic shrinkage and amygdala hyperactivity (Salim, 2016). Moreover, oxidative damage to the hippocampus might disrupt the neural circuitry involved in anxiety and fear conditioning (Hassan et al, 2014).…”

Section: Discussionmentioning

confidence: 99%

Severity of anxiety– but not depression– is associated with oxidative stress in Major Depressive Disorder

Steenkamp

Hough

Reus

et al. 2017

Journal of Affective Disorders

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Background Oxidative stress is implicated in both depression and anxiety, but it is currently unclear whether this relates to syndromal diagnoses or trans-diagnostic dimensional symptoms. We examined the relationship between oxidative stress and severity of depression and anxiety symptoms in individuals with Major Depressive Disorder (MDD). Methods Plasma oxidative stress markers F2-isoprostanes and oxidized glutathione (GSSG), and the antioxidant reduced glutathione (GSH), were assessed in 69 physically healthy, medication-free MDD subjects. Symptoms of anxiety and depression were assessed using the Hamilton Anxiety (HAM-A) and Hamilton Depression (HAM-D) Rating Scales. Total HAM-A and HAM-D scores, along with “core” anxiety and depression subscales, and individual HAM-D items “psychic anxiety” and “depressed mood,” were related to oxidative stress markers. Analyses controlled for age, sex, BMI, and smoking. Results Total HAM-A ratings were positively associated with F2-isoprostanes (β=.26, p=0.042) and GSSG (β=.25, p=0.049), but not GSH (β=.05, p=0.711). Core anxiety severity was positively associated with F2-isoprostanes (β=.34, p=0.012) and GSSG, although this did not reach significance (β=.24, p=0.074). None of the biological markers were significantly associated with total HAM-D or core depression ratings (all p>0.13). Subjects scoring high on “psychic anxiety” had elevated F2-isoprostanes (p=0.030) and GSSG (p=0.020). This was not seen with “depressed mood” scores (all p>0.12). Limitations We assessed peripheral oxidative markers, but their relationship to the brain is unclear. Conclusions Oxidative stress is more closely related to anxiety than depression symptoms in MDD. This highlights the importance of relating oxidative stress to specific symptoms and could provide new insights into the biological correlates of affective disorders.

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“…The rest of the pathways falls into the following categories: (i) cell morphogenesis and cell-cell adhesion; (ii) extracellular matrix; (iii) cell migration; (iv) post-translational modification; (v) nervous system development and signaling (axon guidance, axonogenesis, neurite development, neuron development, neuron differentiation, generation of neurons, and neurogenesis), and (vi) general signaling (G alpha I signaling events, response to biotic stimulus, and G protein coupled receptor activity). While these pathways can be activated by a wide range of conditions, one thing in common is: they can all be activated by intracellular stresses, particularly oxidative stress [20][21][22], and associated damages. Actually, all these pathways are strongly associated with responses to Fenton reactions as noted in our previous study [23].…”

Section: Resultsmentioning

confidence: 99%

Transcription regulation by DNA methylation under stressful conditions in human cancer

Cao

Zhou

et al. 2017

Quant. Biol.

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Background: We aim to address one question: do cancer vs. normal tissue cells execute their transcription regulation essentially the same or differently, and why? Methods: We utilized an integrated computational study of cancer epigenomes and transcriptomes of 10 cancer types, by using penalized linear regression models to evaluate the regulatory effects of DNA methylations on gene expressions. Results: Our main discoveries are: (i) 56 genes have their expressions consistently regulated by DNA methylation specifically in cancer, which enrich pathways associated with micro-environmental stresses and responses, particularly oxidative stress; (ii) the level of involvement by DNA methylation in transcription regulation increases as a cancer advances for majority of the cancer types examined; (iii) transcription regulation in cancer vs. control tissue cells are substantially different, with the former being largely done through direct DNA methylation and the latter mainly done via transcriptional factors; (iv) the altered DNA methylation landscapes in cancer vs. control are predominantly accomplished by DNMT1, TET3 and CBX2, which are predicted to be the result of persistent stresses present in the intracellular and micro-environments of cancer cells, which is consistent with the general understanding about epigenomic functions. Conclusions: Our integrative analyses discovered that a large class of genes is regulated via direct DNA methylation of the genes in cancer, comparing to TFs in normal cells. Such genes fall into a few stress and response pathways. As a cancer advances, the level of involvement by direct DNA methylation in transcription regulation increases for majority of the cancer types examined.

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Oxidative Stress and the Central Nervous System

Cited by 965 publications

References 95 publications

Panax notoginseng saponins suppress lipopolysaccharide‐induced barrier disruption and monocyte adhesion on bEnd.3 cells via the opposite modulation of Nrf2 antioxidant and NF‐κB inflammatory pathways

Panax notoginseng saponins suppress lipopolysaccharide‐induced barrier disruption and monocyte adhesion on bEnd.3 cells via the opposite modulation of Nrf2 antioxidant and NF‐κB inflammatory pathways

Severity of anxiety– but not depression– is associated with oxidative stress in Major Depressive Disorder

Transcription regulation by DNA methylation under stressful conditions in human cancer

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