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Abdi Brandt posted an update 6 months, 2 weeks ago
ulates the antioxidant capacity is compromised. In this context, redox imbalance takes place, resulting in oxidative damage to both lipids (70%, p less then 0.001) and proteins (140%, p less then 0.001). These results suggest that glaucoma damages not only eye structures but also brain visual targets such as the primary visual cortex. Redox imbalance takes place due to an enhancement in ROS and reactive nitrogen species production from different sources, such as NOX family and iNOS, respectively, in an onset where the antioxidant defenses are overwhelmed due to an impaired Nrf2 signaling, leading to oxidative damage to macromolecules.
Degenerative ocular disorders like age-related macular degeneration (AMD) are associated with long-term pro-inflammatory signals on retinal pigment epithelial (RPE) cells. In this study, we investigated the effect of long term treatment of RPE cells with agonists of toll-like receptor (TLR) -3 (Polyinosinicpolycytidylic acid, Poly IC), TLR-4 (lipopolysaccharide, LPS) and the pro-inflammatory cytokine TNFα.
All tests were conducted with primary porcine RPE. Cells were stimulated with Poly IC (1, 10, 100μg/ml), LPS (0.1, 1, 10μg/ml) or TNFα (12.5, 25 or 50ng/ml) for 1 day, 7 days or 4 weeks. Cell viability tests (MTT) were additionally tested in ARPE-19cells. Cytokine secretion (IL-6, IL-1β, IL-8, TNFα, TGF-β) was tested in ELISA, phagocytosis in a microscopic assay, and expression of RPE65 in Western blot. Barrier function was tested in transwell-cultured cells by measuring transepithelial resistance for up to 3 days.
LPS and TNFα significantly reduce cell viability after 1 day and 7 days, Poly IC after mmatory cytokines and therefore may contribute directly to atrophic changes in AMD.Metabolic labeling, in which substrate analogs containing diminutive tags can infiltrate biosynthetic pathways and generate labeled products in cells, has led to dramatic advancements in the means by which complex biomolecules can be detected and biological processes can be elucidated. Within this realm, metabolic labeling of lipid products, particularly in a manner that is headgroup-specific, brings about a number of technical challenges including the complexity of lipid metabolic pathways as well as the simplicity of biosynthetic precursors to headgroup functionality. As such, only a handful of strategies for metabolic labeling of lipids have thus far been reported. However, these approaches provide enticing examples of how strategic modifications to substrate structures, particularly by introducing clickable moieties, can enable the hijacking of lipid biosynthesis. Furthermore, early work in this field has led to an explosion in diverse applications by which these techniques have been exploited to answer key biological questions or detect and track various lipid-containing biological entities. In this article, we review these efforts and emphasize recent advancements in the development and application of lipid metabolic labeling strategies.C5a is a crucial terminal effector of the C cascade, mostly involved in pain and neuroinflammatory conditions. DF3016A is a novel potent and selective C5a receptor (C5aR) inhibitor that crosses the blood-brain barrier (BBB) and may have pharmacological properties. We have previously demonstrated a protective effect of DF3016A on injured primary cortical neurons by oxygen-glucose deprivation-reoxygenation (OGD/R) model to mimic the neuroinflammatory process. Here, we investigated the molecular pathway and factors involved in the neuroprotection previously reported. Our findings show that DF3016A protects against the neuroinflammatory insult by activating brain-derived neurotrophic factor (BDNF) transcription pathway, which involves methyl CpG-binding protein 2 (MeCP2) and microRNA-132 (miR-132) regulatory factors, both required in nociceptive signaling and neuroinflammation. Further in vivo investigations will confirm the functionality of the DF3016A molecule as a therapeutic resource in neuroinflammation and pain injuries.Estrogen replacement therapy decreases some risk factors of the metabolic syndrome but increases the risk of some types of cancer. Tibolone (TIB) has shown similar neuroprotective effects as estrogens. This study aimed to evaluate the effects of TIB on metabolic parameters and the expression of sex hormone receptors in the CNS in ovariectomised rats fed with a hypercaloric diet. Sprague-Dawley female rats were ovariectomised and fed for 30 days with a standard diet (SD) or high-fat high-fructose diet (HFFD) and treated with TIB (1 mg/kg) or vehicle. At the end of the treatments, HFFD increased body weight, glucose tolerance, triglycerides and cholesterol levels, while TIB treatment decreased these parameters. Subsequently, the hippocampus, the hypothalamus and the frontal cortex were dissected. RT-PCR was performed for progesterone receptor (PR), androgen receptor (AR), estrogen receptors alpha and beta (ERα, ERβ), insulin receptor (IR) and insulin-like growth factor 1 (IGF-1). HFFD altered the expression of sex hormone receptors in specific brain structures involved in the regulation of homeostasis and cognition, which highlights the importance of a healthy diet. In turn, TIB modulated the expression of these receptors, particularly in the hypothalamus.Motor- and pain-related processes separately induce a reduction in alpha and beta power. When movement and pain occur simultaneously but are independent of each other, the effects on alpha and beta power are additive. It is not clear whether this additive effect is evident during motor-evoked pain in individuals with chronic pain. We combined highdensity electroencephalography (EEG) with a paradigm in which motor-evoked pain was induced during a jaw force task. selleck compound Participants with chronic jaw pain and pain-free controls produced jaw force at 2% and 15% of their maximum voluntary contraction. The chronic jaw pain group showed exacerbated motor-evoked pain as force amplitude increased and showed increased motor variability and motor error irrespective of force amplitude. The chronic jaw pain group had an attenuated decrease in power in alpha and lower-beta frequencies in the occipital cortex during the anticipation and experience of motor-evoked pain. Rather than being additive, motor-evoked pain attenuated the modulation of alpha and beta power, and this was most evident in occipital cortex.
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