GSNO może m.in. zmniejszać ilość nadtlenoazotynu (https://pl.wikipedia.org/wiki/Reaktywne_formy_azotu).
http://bmcneurosci.biomedcentral.com/ar ... 015-0179-x"Redox-modulating agent of the NO metabolome, S-nitrosoglutathione (GSNO), confers neurovascular protection by reducing the levels of peroxynitrite, a product of aberrant NOS activity."
"GSNO treatment of IR animals decreased IR-activated nNOS activity and neuronal peroxynitrite levels by reducing nNOS phosphorylation at Ser1412. The Ser1412 phosphorylation is associated with increased nNOS activity. Supporting the notion that nNOS activity and peroxynitrite are deleterious following IR, inhibition of nNOS by its inhibitor 7-nitroindazole or reducing peroxynitrite by its scavenger FeTPPS decreased IR injury. GSNO also decreased the activation of AMP Kinase (AMPK) and its upstream kinase LKB1, both of which were activated in IR brain."
"Taken together, these results indicate an injurious nNOS/peroxynitrite/AMPK cycle following stroke, and GSNO treatment of IR inhibits this vicious cycle, resulting in neuroprotection and improved neurological function. GSNO is a natural component of the human body, and its exogenous administration to humans is not associated with any known side effects."
http://journals.plos.org/plosone/articl ... ne.0153716"The present study suggests that the protective effect of GSNO on the alveolar bone resorption is at least in part due to its anti-inflammatory, anti-oxidant and immunomodulatory properties. We demonstrated that the HPMC/GSNO 10 mM solution significantly reduced the TNF-α mRNA in gingival tissue of animals treated with this formulation as well as the gingival levels of TNF-α and IL-1β, when compared with the control HPMC solution group."
"Topical application of HMPC/GSNO 10 mM solution attenuated the gingival oxidative stress, reestablishing the levels of GSH and decreasing nitrotyrosine expression and MDA concentration. Together, these results suggest that the protective effect of the HPMC/GSNO solution is at least partially related to its inhibitory effect on oxidative stress. Moreover, other studies have indicated that GSNO decreases the formation of nitrotyrosine and lipid peroxidation in blood, increasing the reduced GSH/oxidized GSH (GSH/GS-SG) ratio in the brain [39–41]."
https://www.infona.pl/resource/bwmeta1. ... 2fdd5d3aac"We have previously reported that treatment of rats subjected to permanent bilateral common carotid artery occlusion (pBCCAO), a model of chronic cerebral hypoperfusion (CCH), with S-nitrosoglutathione (GSNO), an endogenous nitric oxide carrier, improved cognitive functions and decreased amyloid-β accumulation in the brains. Since CCH has been implicated in tau hyperphosphorylation induced neurodegeneration, we investigated the role of GSNO in regulation of tau hyperphosphorylation in rat pBCCAO model. The rats subjected to pBCCAO had a significant increase in tau hyperphosphorylation with increased neuronal loss in hippocampal/cortical areas. GSNO treatment attenuated not only the tau hyperphosphorylation, but also the neurodegeneration in pBCCAO rat brains. The pBCCAO rat brains also showed increased activities of GSK-3β and Cdk5 (major tau kinases) and GSNO treatment significantly attenuated their activities. GSNO attenuated the increased calpain activities and calpain-mediated cleavage of p35 leading to production of p25 and aberrant Cdk5 activation. In in vitro studies using purified calpain protein, GSNO treatment inhibited calpain activities while 3-morpholinosydnonimine (a donor of peroxynitrite) treatment increased its activities, suggesting the opposing role of GSNO vs. peroxynitrite in regulation of calpain activities. In pBCCAO rat brains, GSNO treatment attenuated the expression of inducible nitric oxide synthase (iNOS) expression and also reduced the brain levels of nitro-tyrosine formation, thereby indicating the protective role of GSNO in iNOS/nitrosative-stress mediated calpain/tau pathologies under CCH conditions. Taken together with our previous report, these data support the therapeutic potential of GSNO, a biological NO carrier, as a neuro- and cognitive-protective agent under conditions of CCH."
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2777134/GSNO is a promising candidate to be evaluated in humans after brain trauma because it not only protects the traumatic penumbra from secondary injury and improves overall tissue structure but also maintains the integrity of BBB and reduces neurologic deficits following CCI in a rat model of experimental TBI.