(+)-Pentazocine reduces oxidative stress and apoptosis in microglia following hypoxia/reoxygenation injury

Heiss, Kathrin; Vanella, Luca; Murabito, Paolo; Prezzavento, Orazio; Marrazzo, Agostino; Castracani, Carlo Castruccio; Barbagallo, Ignazio; Zappalà, Agata; Arena, Elena; Astuto, Marinella; Giarratano, Antonino; Volti, Giovanni Li

doi:10.1016/j.neulet.2016.05.025

Cited by 10 publications

(5 citation statements)

References 18 publications

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“…Although SOD is described as the first important shield against superoxide radicals, the glutathione system is, likewise, an important antioxidant defense. For example, there is evidence that the oxidative stress induced by hypoxia is primarily due to a decrease in GSH levels [40,41]. In this study, we found a significant and greater increase of GR activity after physical exercise in young, sedentary, severely obese volunteers, but not in overweight/moderately obese or normal weight subjects.…”

Section: Discussionsupporting

confidence: 44%

Effects of acute physical exercise on oxidative stress and inflammatory status in young, sedentary obese subjects

et al. 2017

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Circulating oxidative stress and pro-inflammatory markers change after regular physical exercise; however, how a short session of acute physical activity affects the inflammatory status and redox balance in sedentary individuals is still unclear. Aim of this study is to assess antioxidant and inflammatory parameters, both at rest and after acute exercise, in sedentary young men with or without obesity. Thirty sedentary male volunteers, aged 20–45 (mean age 32 ± 7 years), were recruited, divided into 3 groups (normal weight: BMI < 25 kg/m2; overweight to moderate obesity: 25–35 kg/m2; severe obesity: 35–40 kg/m2), and their blood samples collected before and after a 20-min run at ~ 70% of their VO2max for the measurement of Glutathione Reductase, Glutathione Peroxidase, Superoxide Dismutase, Total Antioxidant Status (TAS) and cytokines (IL-2, IL-4, IL-6, IL-8, IL-10, IL-1α, IL-1β, TNFα, MCP-1, VEGF, IFNγ, EGF). Inter-group comparisons demonstrated significantly higher Glutathione Reductase activity in severely obese subjects in the post-exercise period (P = 0.036), and higher EGF levels in normal weight individuals, either before (P = 0.003) and after exercise (P = 0.05). Intra-group comparisons showed that the acute exercise stress induced a significant increase in Glutathione Reductase activity in severely obese subjects only (P = 0.007), a significant decrease in MCP-1 in the normal weight group (P = 0.02), and a decrease in EGF levels in all groups (normal weight: P = 0.025, overweight/moderate obesity: P = 0.04, severe obesity: P = 0.018). Altogether, these findings suggest that in sedentary individuals with different ranges of BMI, Glutathione Reductase and distinct cytokines are differentially involved into the adaptive metabolic changes and redox responses induced by physical exercise. Therefore, these biomarkers may have the potential to identify individuals at higher risk for developing diseases pathophysiologically linked to oxidative stress.

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Section: Discussionsupporting

confidence: 44%

Effects of acute physical exercise on oxidative stress and inflammatory status in young, sedentary obese subjects

et al. 2017

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“…The finding was not consistent with the report that (+)-pentazocine, a Sig-1R agonist, suppressed the microglia activation via inhibition of LPS-induced MAPK/ERK pathway in retinal microglia (Zhao et al, 2014 ). Moreover, (+)-pentazocine only at certain doses (1 μM and 10 μM) reduced apoptotic cell death via ERK1/2 pathway in BV2 microglia under hypoxia/reoxygenation conditions (Heiss et al, 2016 ). This is interesting because it suggests that allosteric modulator of Sig-1R modulate microglia-mediated neuroinflammation via different mechanism from the receptor agonist.…”

Section: Sigma-1 Receptor and Microgliamentioning

confidence: 99%

Sigma-1 Receptor-Modulated Neuroinflammation in Neurological Diseases

Jia

Cheng

Wang

et al. 2018

Front. Cell. Neurosci.

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A large body of evidence indicates that sigma-1 receptors (Sig-1R) are important drug targets for a number of neuropsychiatric disorders. Sig-1Rs are enriched in central nervous system (CNS). In addition to neurons, both cerebral microglia and astrocytes express Sig-1Rs. Activation of Sig-1Rs is known to elicit potent neuroprotective effects and promote neuronal survival via multiple mechanisms, including promoting mitochondrial functions, decreasing oxidative stress and regulating neuroimmnological functions. In this review article, we focus on the emerging role of Sig-1Rs in regulating neuroinflammation and discuss the recent advances on the Sig-1R-modulating neuroinflammation in the pathophysiology and therapy of neurodegenerative disorders.

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“…For instance, administration of a potent allosteric S1R modulator, SKF83959 significantly reduces the release of NOS as well as the expression of pro-inflammatory cytokines, such as TNFα, IL1β, and iNOS in LPS-stimulated microglial cells in vitro [66]. Interestingly, these effects were reversed by administration of a selective S1R antagonist (BD1047) [66], supporting the key role of S1Rs in mediating the anti-inflammatory effects of microglia [65,67,68]. The progesterone receptor membrane component-1 (PGRMC1) interacts with S2R to regulate microglial cell activity, and modulates axonal sprouting [69,70].…”

Section: Mechanisms Regulating Microglial Cell Activitymentioning

confidence: 86%

Role of Microglia in Modulating Adult Neurogenesis in Health and Neurodegeneration

Al‐Onaizi

Al-Khalifah

Qasem

et al. 2020

IJMS

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Microglia are the resident immune cells of the brain, constituting the powerhouse of brain innate immunity. They originate from hematopoietic precursors that infiltrate the developing brain during different stages of embryogenesis, acquiring a phenotype characterized by the presence of dense ramifications. Microglial cells play key roles in maintaining brain homeostasis and regulating brain immune responses. They continuously scan and sense the brain environment to detect any occurring changes. Upon detection of a signal related to physiological or pathological processes, the cells are activated and transform to an amoeboid-like phenotype, mounting adequate responses that range from phagocytosis to secretion of inflammatory and trophic factors. The overwhelming evidence suggests that microglia are crucially implicated in influencing neuronal proliferation and differentiation, as well as synaptic connections, and thereby cognitive and behavioral functions. Here, we review the role of microglia in adult neurogenesis under physiological conditions, and how this role is affected in neurodegenerative diseases.

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(+)-Pentazocine reduces oxidative stress and apoptosis in microglia following hypoxia/reoxygenation injury

Cited by 10 publications

References 18 publications

Effects of acute physical exercise on oxidative stress and inflammatory status in young, sedentary obese subjects

Effects of acute physical exercise on oxidative stress and inflammatory status in young, sedentary obese subjects

Sigma-1 Receptor-Modulated Neuroinflammation in Neurological Diseases

Role of Microglia in Modulating Adult Neurogenesis in Health and Neurodegeneration

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