NO signaling in the CNS: from the physiological to the pathological

Bishop, Amy; Anderson, James

doi:10.1016/j.tox.2004.11.034

Cited by 96 publications

(79 citation statements)

References 74 publications

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“…With these findings displaying the prolidase level not decreasing in the vitamin C group and significantly decreasing in the lipoic acid and the combination group, suggests that lipoic acid has a positive effect on wound healing through decreasing the prolidase level through inhibiting nitric oxide, and that prolidase can be used as a wound healing parameter. This is consistent with the statement in the literature that nitric oxide is one of the regulators of prolidase enzyme, which is also a free radical, and nitric oxide is reported to stimulate prolidase activity (24). It has been demonstrated that the nitric acid synthase enzyme is also activated during ischemia-reperfusion injury and abundant nitric oxide leads to bacterial translocation through impairing the barrier function of the intestine (25).…”

Section: Discussionsupporting

confidence: 91%

Comparison of the Effects of Alpha Lipoic Acid and Vitamin C on Colonic Anastomosis in the Rat Sepsis Model

et al. 2014

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Section: Discussionsupporting

confidence: 91%

Comparison of the Effects of Alpha Lipoic Acid and Vitamin C on Colonic Anastomosis in the Rat Sepsis Model

et al. 2014

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“…Although NO functions as an important molecule in various biological processes (39,41,42), its role in immune regulation is not fully understood. For example, NO can function as a cytotoxic molecule and high levels of NO may be detrimental to animals and contribute to autoimmune diseases (48,49), yet it can be critical for the protection of hosts to infections (40,41).…”

Section: Discussionmentioning

confidence: 99%

Regulatory T Cells Can Mediate Their Function through the Stimulation of APCs to Produce Immunosuppressive Nitric Oxide

Chen

Lee

Zhong

et al. 2006

The Journal of Immunology

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Regulatory T cells (Tr cells) play a critical role in inducing immune tolerance. It remains largely unclear how various types of Tr cells perform their regulatory function. We have studied the underlying regulatory mechanism of a population of autoantigen-specific CD4+ Tr cells. These T cells are specific for the glutamic acid decarboxylase p206–220 peptide and are isolated from the diabetes-resistant nonobese-resistant mice. Although these T cells express T-bet and display a Th1 phenotype, they are able to inhibit diabetes. Their regulatory function is dependent on both IFN-γ and cell contact with target cells. These Tr cells can mediate their cell contact-dependent regulatory function by secreting IFN-γ which stimulates APCs to produce NO. NO is necessary for the Tr cells to inhibit the proliferation of pathogenic T cells and the development of diabetes. Therefore, we have identified a novel mechanism by which these Tr cells can exert their regulatory function. These results also provide an explanation as to why IFN-γ may play both pathogenic and immunomodulatory roles in autoimmune diseases.

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“…Free iron production by HO-1 is also associated with an up-regulation of an iron pump which increases intracellular iron efflux, thereby making iron available as an essential cofactor for numerous cellular enzymes and redox-dependent proteins [37]. Furthermore, HO-1-derived CO has been demonstrated to be an important cellular messenger and regulatory molecule in a variety of physiologic functions, much as NO is [41,42]. The signaling functions of CO are similar to NO except that NO forms the radicals peroxynitrite and superoxide, which are cytotoxic [43][44][45].…”

Section: Discussionmentioning

confidence: 99%

Ketamine-Induced Gastroprotection During Endotoxemia: Role of Heme-Oxygenase-1

2006

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Inducible nitric oxide synthase contributes to lipopolysacharide-induced gastric injury. In contrast, heme-oxygenase-1 has anti-inflammatory effects and is protective against oxidative tissue injury. Ketamine attenuates injury from lipopolysacharide and is associated with changes in oxidative stress proteins, but its effects on the stomach remain to be fully elucidated. We hypothesized that ketamine would diminish gastric injury from lipopolysacharide via down-regulation of nuclear factor-kappass, activator protein-1, and inducible nitric oxide synthase, as well as up-regulation of heme-oxygenase-1. Ketamine up-regulated heme-oxygenase-1 and attenuated lipopolysacharide-induced changes in gastric nuclear factor-kappass, activator protein-1, and inducible nitric oxide synthase. Ketamine negated LPS-induced gastric injury from acidified ethanol, an effect reversed by tin protoporphorin IX. Ketamine diminishes the susceptibility of gastric mucosa to damage from luminal irritants during endotoxemia, which is mediated in part by down-regulation of iNOS and up-regulation of HO-1.

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NO signaling in the CNS: from the physiological to the pathological

Cited by 96 publications

References 74 publications

Comparison of the Effects of Alpha Lipoic Acid and Vitamin C on Colonic Anastomosis in the Rat Sepsis Model

Comparison of the Effects of Alpha Lipoic Acid and Vitamin C on Colonic Anastomosis in the Rat Sepsis Model

Regulatory T Cells Can Mediate Their Function through the Stimulation of APCs to Produce Immunosuppressive Nitric Oxide

Ketamine-Induced Gastroprotection During Endotoxemia: Role of Heme-Oxygenase-1

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