Inosine and guanosine preserve neuronal and glial cell viability in mouse spinal cord cultures during chemical hypoxia

Litsky, Monica L.; Hohl, Charlene M.; Lucas, Jen Hill; Jurkowitz, Marianne S.

doi:10.1016/s0006-8993(99)01086-0

Cited by 82 publications

(57 citation statements)

References 26 publications

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“…19,20 Inosine is also capable of protecting astrocytes and neurons against hypoxia, ischemia and zinc sulfate in vitro. 15,18,29 The present study demonstrated that inosine could reduce apoptosis after crushing injury of the spinal cord. Secondary degeneration has been attributed to a number of mechanisms underlying cell death, including ATPdepletion, free radical overproduction, oxidative damage, cytokines and inflammation.…”

Section: Discussionsupporting

confidence: 61%

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Secondary degeneration reduced by inosine after spinal cord injury in rats

et al. 2005

Spinal Cord

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Study design: Assessment of the potential protective effects of inosine on an animal model of spinal cord injury. Objectives: Our previous studies have demonstrated that inosine can directly protect neurons in vitro from zinc-induced injury and axotomized retinal ganglion cells of rats in vivo. This investigation was carried out to examine the possible protective effects of inosine on spinal cord secondary degeneration. Setting: Institute of Neurosciences, The Fourth Military Medical University, Xi'an, China. Methods: Compressive spinal cord injury (95-g load for 1 min) model was established in rats, and inosine was administrated beginning at different time points (2, 12, or 24 h) after spinal cord injury. Results: Using terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end labeling (TUNEL) technique and hematoxylin and eosin staining, our study demonstrated that administration of inosine as late as 12 h after injury significantly reduced the total volume of spinal cord degenerative areas and the number of apoptotic cells 3 days following the trauma. Conclusion: Inosine can significantly reduce the spread of secondary degeneration and the cell death following spinal cord injury in adult rats. These findings may find a clinical application in the treatment of acute spinal cord injury.

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Section: Discussionsupporting

confidence: 61%

“…[13][14][15][16][17][18][19][20][21] These effects kindle the hope for its use in SCI to conquer secondary degeneration. The aim of the present study was to investigate the possible neuroprotective and ameliorating effects and the time window of inosine in an experimental spinal cord clip compression injury model in adult rats.…”

Section: Introductionmentioning

confidence: 99%

Secondary degeneration reduced by inosine after spinal cord injury in rats

et al. 2005

Spinal Cord

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“…Recent studies have reported a protective effect of guanosine against neuronal hypoxic injury in culture (24,25). This beneficial effect was ascribed to an enhancement in ATP production.…”

Section: Discussionmentioning

confidence: 99%

Guanosine supplementation reduces apoptosis and protects renal function in the setting of ischemic injury

Kelly¹,

Plotkin²,

Dagher³

2001

J. Clin. Invest.

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“…Inosine was also shown to reduce ischemic brain injury in rats (Shen et al 2005 ) . Inosine and Guo preserved the viability of cultured astrocytes, neurons (Jurkowitz et al 1998 ;Litsky et al 1999 ) , and brain slices maintained under hypoxic or hypoglycemic conditions (Frizzo et al 2002 ) . The potential neuroprotective effects of Guo are also supported by the fi nding that neuronal and astrocytic cell cultures are able to release Guo and Ado under both basal and ischemic conditions .…”

Section: Strokementioning

confidence: 99%

Anatomical Distribution of Nucleoside System in the Human Brain and Implications for Therapy

Kovács

Dobolyi

2012

Adenosine

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Nucleosides have a wide range of physiological and pathophysiological roles in the human brain as modulators of a variety of neural functions. For example, adenosine, inosine, guanosine, and uridine participate in the mechanisms underlying memory, cognition, sleep, pain, depression, schizophrenia, epilepsy, Alzheimer's disease, Huntington's disease, and Parkinson's disease. Consequently, increasing attention is now being given to the speci fi c role of nucleosides in physiological and pathological processes in the human brain. Different elements of nucleoside system, including nucleoside concentrations, metabolic enzyme activity, and expression of nucleoside transporters and receptors, may be changed under normal and pathological conditions. The alterations suggest that interlinked elements of the nucleoside system are functioning in a tightly concerted manner.Nucleoside levels, activity of nucleoside metabolic enzymes, and expression of nucleoside transporters and receptors are unevenly distributed in the brain, suggesting that nucleosides have different roles in functionally distinct human brain areas. The aim of this chapter is to summarize our present knowledge of the anatomical distribution of nucleoside system in the human brain, placing emphasis on potential therapeutic pharmacological strategies.

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Inosine and guanosine preserve neuronal and glial cell viability in mouse spinal cord cultures during chemical hypoxia

Cited by 82 publications

References 26 publications

Secondary degeneration reduced by inosine after spinal cord injury in rats

Secondary degeneration reduced by inosine after spinal cord injury in rats

Guanosine supplementation reduces apoptosis and protects renal function in the setting of ischemic injury

Anatomical Distribution of Nucleoside System in the Human Brain and Implications for Therapy

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