Gingko biloba Extract Inhibits Oxidative Stress and Ameliorates Impaired Glial Fibrillary Acidic Protein Expression, but Can Not Improve Spatial Learning in Offspring from Hyperhomocysteinemic Rat Dams

Abstract

We aimed to study the effects of gingko biloba extract (EGb) on oxidative stress, astrocyte maturation and cognitive disfunction in offspring of hyperhomocysteinemic rats. Hyperhomocysteinemia was induced in the pregnant rats by administration of methionine (1 gr/kg body weight) dissolved in drinking water throughout pregnancy. One group of animals has received same amount of methionine plus 100 mg/kg/day EGb during pregnancy. On the postnatal day 1, half of the pups from all groups were sacrificed to study the lipid peroxidation (LPO) in different subfractions of brain. Other half of pups were tested in Morris water maze to assess differences in learning and memory performance at the 75 days of age. Maternal hyperhomocysteinemia significantly increased LPO levels especially in mitochondrial subfraction of fetal pup brains. EGb significantly prevented this LPO inrease. Methionine administration to animals reduced glial fibrillary acidic protein (GFAP) expression in pup brains significantly. EGb administration improved GFAP expression significantly. Offspring of hyperhomocysteinemic animals had poor long term spatial memory performance on Morris water maze and EGb administration had no effect on impaired spatial memory. In conclusion, maternally induced hyperhomocysteinemia significantly increased oxidative stress, decreased expression of GFAP and impaired learning performance.

Low doses of imidacloprid induce disruption of intercellular adhesion and initiate proinflammatory changes in Caco-2 cells

“…Therefore, low doses of imidacloprid may suppress the enterocyte viability and induce the redox imbalance. It should be mentioned that redox imbalance is not specific to neonicotinoid's toxicity and the oxidative stress generation was detected in a large number of cytotoxicity models for different kinds of pollutants (Koz et al, 2011;Nedzvetskii et al, 2012).…”

Targetable Fluorescent Probe for Monitoring Exogenous and Endogenous NO in Mitochondria of Living Cells

“…24,25 Finally, NO and oxidation product ONOO − in mitochondria can easily diffuse into other subcellular structures such as lysosomes and lipid membrane and be a well-known inflammatory mediator in regulating of autophagy. 26−28 Although studies of mitochondrial NO have helped people to understand many NO-relative physiological processes such as aging of the cardiovascular system, 29 fatty livers, 30 and lipid peroxidation of the brain, 31 unknown functions of mitochondrial NO and the dependency relationship of NO with calcium ions and copper(I) in mitochondria is still not well established. 32−34 Since there remain many other aspects awaiting discovery, it is very meaningful for NO chemical biology to search for methods and tools to monitor mitochondrial NO.…”

Citicoline affects serum angiostatin and neurospecific protein levels in patients with atrial fibrillation and ischemic stroke

“…Therefore, serum GFAP can be utilized as a marker of astrocytic reactivity levels. Some researchers have shown that GFAP levels increase in patients with acute cerebral infarction and that this increase is proportional to the extent of the lesion and the severity of the infarct [16,18]. Analogically, serum NF proteins, expressed exclusively in neurons, are blood biomarker candidates indicative of neuronal atrophy and axonal injury occurring in various neurodegenerative conditions and brain traumas [20].…”

“…Among all CNS molecules, specific cytoskeletal proteins are the most reliable candidates for the role of biomarkers of brain injury because of their exclusive expression in neurons or glial cells and relative stability to proteolytic degradation in the bloodstream [15]. Numerous studies indicate that glial fibrillary acidic protein (GFAP), a specific protein of astroglial cells, can serve as a sensitive and valuable marker for brain damage as well as an index of neuroprotective efficacy [16]. After cerebral ischemia, astrocytes undergo a vigorous response called astrogliosis characterized by increasingly higher GFAP expression.…”

“…However, reactive astrocytes can form a glial scar that obstructs axonal regeneration and communication [17]. In humans, elevated serum GFAP concentrations reflect astrogliosis induced by intracerebral hemorrhage, acute cerebral stroke and traumatic brain injury, when GFAP moves into the circulation via the damaged BBB [16,18]. Neuron derived markers of ischemic stroke can be represented by neurofilament (NF) proteins, which are known as highly specific constituents of neuronal intermediate filaments and play an important role in the modulation of axonal calibre and transport.…”