Preservation of neurological functions by nitric oxide synthase inhibitors in conscious rats following delayed hemorrhagic shock

Shirhan, Md.; Moochhala, Shabbir; Yang, Kerwin Low Siew; Sng, Judy; Ng, Kian Chye; Mok, Pamela; Lu, Jia

doi:10.1016/j.lfs.2004.07.015

Cited by 7 publications

(2 citation statements)

References 24 publications

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“…For example, robust iNOS expression is induced in microglia, astrocytes and neurons of ischemic brain [17][18][19]. Studies with iNOS inhibitors and iNOS knockout mice confirm that a decreased iNOS activity can reduce ischemic brain injury [9,[20][21][22][23][24][25][26]. However, iNOS has been shown to participate in induction of ischemic tolerance [27,28] and neurogenesis after brain ischemia [13].…”

Section: Discussionmentioning

confidence: 99%

RNA interference‐produced autoregulation of inducible nitric oxide synthase expression

2011

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Vector-mediated delivery of short-hairpin RNA (shRNA) to regulate gene expression holds a great therapeutic promise. We hypothesize that gene expression can be autoregulated with RNA interference. We used inducible nitric oxide synthase (iNOS) as a gene model to test this hypothesis. Lipopolysaccharide dose-dependently increased iNOS in rat aortic smooth muscle cells and the nitrite production from these cells. These increases were attenuated in cells transfected with plasmids containing code for iNOS shRNA whose expression was controlled by an iNOS promoter. The production of shRNA was lipopolysaccharide dose-dependent. The lipopolysaccharide-induced iNOS expression in rat C6 glioma cells also was attenuated by transfection with plasmids containing the iNOS shRNA code. These results provide proof-of-concept evidence for using RNA interference technique to achieve autoregulation of gene expression.

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Section: Discussionmentioning

confidence: 99%

RNA interference‐produced autoregulation of inducible nitric oxide synthase expression

2011

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“…In addition, AG inhibits the inducible isoform of nitric oxide (NO) synthase, an enzyme activated at the transcriptional level by proinflammatory stimuli in the injured brain. Excessive production of NO contributes to neuronal degeneration and secondary damage, and the protective effects of AG have been described in various models of CNS injury (Zimmerman et al ., 1995; Ivanova et al ., 1998; Dogan et al ., 1999; Chatzipanteli et al ., 2002; Lu et al ., 2003; Moochhala et al ., 2004; Shirhan et al ., 2004a).…”

Section: Introductionmentioning

confidence: 99%

Structural and functional recovery elicited by combined putrescine and aminoguanidine treatment after aspirative lesion of the fimbria–fornix and overlying cortex in the adult rat

Muller

Herberth

Cosquer

et al. 2007

Eur J of Neuroscience

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Damage to the adult CNS often causes permanent deficits. Based on a lesion model of septohippocampal pathway aspiration in the rat, we attempted to promote neuronal cell survival and post-traumatic recovery by using a pharmacological treatment combining aminoguanidine and putrescine (AGP). The functional recovery was followed over 15 weeks before morphological analysis. AGP treatment produced a persistent attenuation (approximately 50%) of the lesion-induced hyperactivity, a reduction (approximately 60%) in the sensorimotor impairments and an improved performance in the water-maze task which did not, however, rely upon improved memory capabilities. AGP weakened the lesion-induced decrease in ChAT-positive neurons in the medial septum and the extent of thalamic retrograde necrosis (by approximately 30% in each case) and resulted in a partial cholinergic reinnervation of the dentate gyrus. These promising results support the idea that coadministration of putrescine and aminoguanidine might become a potent way to foster structural and functional recovery (or compensation) in the adult mammalian CNS after injury.

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Inducible nitric oxide synthase inhibitors abolished histological protection by late ischemic preconditioning in rat retina

Sakamoto

Yonoki

Kubota

et al. 2006

Experimental Eye Research

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Preservation of neurological functions by nitric oxide synthase inhibitors in conscious rats following delayed hemorrhagic shock

Cited by 7 publications

References 24 publications

RNA interference‐produced autoregulation of inducible nitric oxide synthase expression

RNA interference‐produced autoregulation of inducible nitric oxide synthase expression

Structural and functional recovery elicited by combined putrescine and aminoguanidine treatment after aspirative lesion of the fimbria–fornix and overlying cortex in the adult rat

Inducible nitric oxide synthase inhibitors abolished histological protection by late ischemic preconditioning in rat retina

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