Regular ArticleIL-6 Deficiency Leads to Reduced Metallothionein-I+II Expression and Increased Oxidative Stress in the Brain Stem after 6-Aminonicotinamide Treatment
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Interleukin-6: Its role and mechanisms in rescuing depression-like behaviors in rat models of depression
2019, Brain, Behavior, and ImmunityCitation Excerpt :In addition, we also found that knocking-down of IL-6 could increase the expression levels of pro-inflammatory cytokines such as the IL-1β, TNF-αand IFN-γ. It has been reported that IL-6 deficiency leads to increased oxidative stress and in the number of apoptotic neurons within the brain, as well as a delay in neural regeneration as compared with that observed in normal mice (Penkowa and Hidalgo, 2000; Penkowa et al., 2000). Thus, these results suggest that tissue damage induced by oxidative stress and apoptosis may result in the production of inflammatory cytokines via feedback mechanisms.
In vivo effect of acute exposure to interleukin-6 on the developing visual system
2019, Neuroscience LettersCitation Excerpt :IL-6 levels are low in physiological conditions [5], but it increases in a number of pathological conditions [5–7]. IL-6 induces neuroprotection [8,9], regeneration of the optic nerve after crushing [10] and it is also important in the mechanism of axonal growth and recovery of function after injury [11,12]. Recently we had demonstrated that an acute intravitreal injection with IL-6 alters the laminar segregation of the uncrossed retinotectal pathway in different stages of development [13].
Exercising the worry away: How inflammation, oxidative and nitrogen stress mediates the beneficial effect of physical activity on anxiety disorder symptoms and behaviours
2013, Neuroscience and Biobehavioral ReviewsCitation Excerpt :However, oxidative damage to IL-6ra subunits leads to decreased STAT-3 and subsequent M-SOD activity. Increased levels of IL-6 can prevent this oxidative damage in a stroke reperfusion model, possibly through modulating gene expression or up-regulating anti-oxidants (Penkowa and Hidalgo, 2000). In another recent study, two weeks of voluntary wheel running in mice protected against hippocampal dentate gyrus apoptosis induced by injection of trimethytin (TMT) (Funk et al., 2011), a substance known to induced cell death via TNF-α receptor activation (Harry et al., 2008).
Cytokines and innate inflammation in the pathogenesis of human traumatic brain injury
2011, Progress in NeurobiologyCitation Excerpt :In the setting of TBI, IL6 has mostly been associated with neuroprotective actions. Using a cryolesion model and genetically manipulated mice, Penkowa and Hidalgo (2000) have described an impaired inflammatory response associated with increased neurodegeneration in IL6 deficient mice. In contrast, decreased oxidative stress and apoptotic cell death, together with increased healing and tissue repair were seen in transgenic mice overexpressing IL6 in astrocytes (Penkowa et al., 2003).
Immune and Inflammatory Responses in the Central Nervous System: Modulation by Astrocytes
2008, NeuroImmune BiologyCitation Excerpt :These mice show chronic neuroinflammation and neurodegeneration, and in the case of the IL-3 and TNF transgenic mice, demyelination and progressive motor disease are also seen [49,50]. In agreement with these in vivo models, it has been demonstrated that IL-6 protects neurons against ischemic damage and excitotoxicity [38–51]; yet, it is also largely responsible for the neuropathology associated with the multiple sclerosis (MS; Fig. 1) animal model, experimental autoimmune encephalomyelitis (EAE), since IL-6 KO mice are completely resistant to EAE [52–55]. Administration of the superantigen staphylococcal enterotoxin B, which acts through a TNF-receptor pathway, overcomes this resistance, but IL-6 is still considered crucial in perpetuating the disease [56].
Psychosocial and biochemical interactions in aging: Preliminary results from an Italian old sample of "Zincage" project
2007, Archives of Gerontology and Geriatrics
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