Octadecaneuropeptide ODN prevents hydrogen peroxide-induced oxidative damage of biomolecules in cultured rat astrocytes

Hamdi, Yosra; Kaddour, Hadhemi; Vaudry, David; Leprince, Jérôme; Zarrouk, Amira; Hammami, Mohamed; Vaudry, Hubert; Tonon, Marie‐Christine; Amri, Mohamed; Masmoudi-Kouki, Olfa

doi:10.1016/j.peptides.2015.06.010

Cited by 27 publications

(18 citation statements)

References 44 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…*p < 0.05; **p < 0.01; different from the control group (Student's t test) DNA damage in the rat cerebellum, probably by GSH depletion. Such damages may contribute to cell fate decision for apoptosis observed in the present report [41].…”

Section: Discussionmentioning

confidence: 53%

See 1 more Smart Citation

D-Galactose Causes Motor Coordination Impairment, and Histological and Biochemical Changes in the Cerebellum of Rats

et al. 2016

View full text Add to dashboard Cite

Classical galactosemia is an inborn error of carbohydrate metabolism in which patients accumulate high concentration of galactose in the brain. The most common treatment is a galactose-restricted diet. However, even treated patients develop several complications. One of the most common symptoms is motor coordination impairment, including affected gait, balance, and speech, as well as tremor and ataxia. In the present study, we investigated the effects of intracerebroventricular galactose administration on motor coordination, as well as on histological and biochemical parameters in cerebellum of adult rats. Wistar rats received 5 μL of galactose (4 mM) or saline by intracerebroventricular injection. The animals performed the beam walking test at 1 and 24 h after galactose administration. Histological and biochemical parameters were performed 24 h after the injections. The results showed motor coordination impairment at 24 h after galactose injection. Galactose also decreased the number of cells in the molecular and granular layers of the cerebellum. The immunohistochemistry results suggest that the cell types lost by galactose are neurons and astrocytes in the spinocerebellum and neurons in the cerebrocerebellum. Galactose increased active caspase-3 immunocontent and acetylcholinesterase activity, decreased acetylcholinesterase immunocontent, glutathione, and BDNF levels, as well as caused protein and DNA damage. Our results suggest that galactose induces histological and biochemical changes in cerebellum, which can be associated with motor coordination impairment.

show abstract

Section: Discussionmentioning

confidence: 53%

“…GSH depletion is involved in the apoptotic processes in both intrinsic and/or extrinsic pathways [39,40]. Also, the depletion of GSH content can cause damage to biomolecules such as proteins and DNA, which contributes to the spread of apoptotic pathways [41].…”

Section: Introductionmentioning

confidence: 99%

D-Galactose Causes Motor Coordination Impairment, and Histological and Biochemical Changes in the Cerebellum of Rats

et al. 2016

View full text Add to dashboard Cite

show abstract

“…2008; Hamdi et al 2015;Liu et al 2013). Various studies indicate that an excess of H 2 O 2 can provoke cell apoptosis via multiple mechanisms, including the stimulation of some pro-apoptotic genes of the Bcl-2 family responsible for the formation of mitochondrial permeability transition pores, a collapse of the mitochondrial membrane potential, and a decrease in ATP generation (Gyulkhandanyan et al 2003;Kaddour et al 2013;Liu et al 2013).…”

Section: Discussionmentioning

confidence: 99%

Involvement of endogenous antioxidant systems in the protective activity of pituitary adenylate cyclase‐activating polypeptide against hydrogen peroxide‐induced oxidative damages in cultured rat astrocytes

Douiri

Bahdoudi

Hamdi

et al. 2016

Journal of Neurochemistry

Self Cite

View full text Add to dashboard Cite

Astroglial cells possess an array of cellular defense mechanisms, including superoxide dismutase (SOD) and catalase antioxidant enzymes, to prevent damages caused by oxidative stress. Nevertheless, astroglial cell viability and functionality can be affected by significant oxidative stress. We have previously shown that pituitary adenylate cyclase-activating polypeptide (PACAP) is a potent glioprotective agent that prevents hydrogen peroxide (H 2 O 2 )-induced apoptosis in cultured astrocytes. The purpose of this study was to investigate the potential protective effect of PACAP against oxidative-generated alteration of astrocytic antioxidant systems.Incubation of cells with subnanomolar concentrations of PACAP inhibited H 2 O 2 -evoked reactive oxygen species accumulation, mitochondrial respiratory burst, and caspase-3 mRNA level increase. PACAP also stimulated SOD and catalase activities in a concentration-dependent manner, and counteracted the inhibitory effect of H 2 O 2 on the activity of these two antioxidant enzymes. The protective action of PACAP against H 2 O 2 -evoked inhibition of antioxidant systems in astrocytes was protein kinase A, PKC, and MAP-kinase dependent. In the presence of H 2 O 2 , the SOD blocker NaCN and the catalase inhibitor 3-aminotriazole, both suppressed the protective effects of PACAP on SOD and catalase

show abstract

“…Downstream of protein kinase A, ODN induces ERK phosphorylation which, in turn, activates the expression of the anti-apoptotic gene Bcl-2 and blocks the stimulation by H 2 O 2 of the proapoptotic gene Bax. The effect of ODN on the Bax/ Bcl-2 balance could possibly explain its antagonism of the deleterious action of H 2 O 2 on mitochondrial membrane integrity and caspase-3 activation (Hamdi et al, 2012(Hamdi et al, , 2015. This anti-apoptotic effect of ODN might be important in neurodegenerative diseases and stroke.…”

Section: Metabotropic Octadecaneuropeptide (Odn) Receptormentioning

confidence: 99%

Astroglia as a cellular target for neuroprotection and treatment of neuro‐psychiatric disorders

Liu

Teschemacher

Kasparov

2017

Glia

View full text Add to dashboard Cite

Astrocytes are key homeostatic cells of the central nervous system. They cooperate with neurons at several levels, including ion and water homeostasis, chemical signal transmission, blood flow regulation, immune and oxidative stress defense, supply of metabolites and neurogenesis. Astroglia is also important for viability and maturation of stem‐cell derived neurons. Neurons critically depend on intrinsic protective and supportive properties of astrocytes. Conversely, all forms of pathogenic stimuli which disturb astrocytic functions compromise neuronal functionality and viability. Support of neuroprotective functions of astrocytes is thus an important strategy for enhancing neuronal survival and improving outcomes in disease states. In this review, we first briefly examine how astrocytic dysfunction contributes to major neurological disorders, which are traditionally associated with malfunctioning of processes residing in neurons. Possible molecular entities within astrocytes that could underpin the cause, initiation and/or progression of various disorders are outlined. In the second section, we explore opportunities enhancing neuroprotective function of astroglia. We consider targeting astrocyte‐specific molecular pathways which are involved in neuroprotection or could be expected to have a therapeutic value. Examples of those are oxidative stress defense mechanisms, glutamate uptake, purinergic signaling, water and ion homeostasis, connexin gap junctions, neurotrophic factors and the Nrf2‐ARE pathway. We propose that enhancing the neuroprotective capacity of astrocytes is a viable strategy for improving brain resilience and developing new therapeutic approaches.

show abstract

Octadecaneuropeptide ODN prevents hydrogen peroxide-induced oxidative damage of biomolecules in cultured rat astrocytes

Cited by 27 publications

References 44 publications

D-Galactose Causes Motor Coordination Impairment, and Histological and Biochemical Changes in the Cerebellum of Rats

D-Galactose Causes Motor Coordination Impairment, and Histological and Biochemical Changes in the Cerebellum of Rats

Involvement of endogenous antioxidant systems in the protective activity of pituitary adenylate cyclase‐activating polypeptide against hydrogen peroxide‐induced oxidative damages in cultured rat astrocytes

Astroglia as a cellular target for neuroprotection and treatment of neuro‐psychiatric disorders

Contact Info

Product

Resources

About