Glia activation and its role in oxidative stress

Abstract

Glia activation and neuroinflamation are major factors implicated in the aetiology of most neurodegenerative diseases (NDDs). Several agents and toxins have been known to be capable of inducing glia activation an inflammatory response; most of which are active substances that can cause oxidative stress by inducing production of reactive oxygen species (ROS). Neurogenesis on the other hand involves metabolic and structural interaction between neurogenic and glia cells of the periventricular zone (PVZ); a region around the third ventricle. This study investigates glia activation (GFAP), cell proliferation (Ki-67) and neuronal metabolism (NSE) during neurogenesis and oxidative stress by comparing protein expression in the PVZ against that of the parietal cortex. Adult Wistar Rats were treated with normal saline and 20 mg/Kg KCN for 7 days. The tissue sections were processed for immunohistochemistry to demonstrate glia cells (anti Rat-GFAP), cell proliferation (anti Rat-Ki-67) and neuronal metabolism (anti Rat-NSE) using the antigen retrieval method. The sections from Rats treated with cyanide showed evidence of neurodegeneration both in the PVZ and cortex. The distribution of glia cells (GFAP), Neuron specific Enolase (NSE) and Ki-67 increased with cyanide treatment, although the increases were more pronounced in the neurogenic cell area (PVZ) when compared to the cortex. This suggests the close link between neuronal metabolism and glia activation both in neurogenesis and oxidative stress.

Aza‐CGP37157‐lipoic hybrids designed as novel Nrf2‐inducers and antioxidants exert neuroprotection against oxidative stress and show neuroinflammation inhibitory properties

“…Proinflammatory signaling and glial activation plays a central role in brain damage in NDDs (Iadecola & Anrather, ; Ogundele et al, ). Proinflammatory signals are initiated in all phases, engaging both the innate and adaptive responses.…”

“…Furthermore, mNCX blockade avoids mitochondrial Ca 2+ depletion and augments ATP synthesis and neuronal viability. On the other hand, OS induces glial activation by several mechanisms inducing the expression of RNS production enzyme iNOS and the release of cytokines (Ogundele et al, ). The interconnection of OS and neuroinflammation generates a vicious cycle, known as chronic neuroinflammation, that leads to extended neuronal damage.…”

Environmental factors in the development and progression of late-onset Alzheimer’s disease

“…At the systemic level, HPA axis dysfunction is the main mechanism to induce a LOAD phenotype by behavioral stress [88,89] . At the intercellular level, cerebrovascular dysfunction, Aβ accumulation [57,90] , glial activation [91][92][93] , and metal toxicity [11][12][13] are generally responsible for an abnormal microenvironment surrounding neurons, and contribute to their dysfunction.…”

“…the main mechanism to induce AD phenotype [42,88,89] . At the intercellular level, cerebrovascular dysfunction, Aβ accumulation [57,90] , glial activation [91][92][93]99] , and metal toxicity [11][12][13] are responsible for creating an abnormal microenvironment around neurons. At the intracellular level, the imbalance between the activities of tau-related kinases and phosphatases [29,94,95] , and abnormal epigenetic modifi cation, especially DNA methylation and histone acetylation [96][97][98] , are associated with neuronal dysfunction in LOAD.…”

Endothelial proliferation modulates neuron-glia survival and differentiation in ischemic stress

“… 15 , 16 , 21 – 24 In addition, our previous findings of glia activation, neuronal degeneration and proliferation induced by differential oxidative stress has revealed that regional differences exists in stress response elicited in the brain; specifically across the plastic and non-plastic brain regions. 25 …”