Protective effects of epigallocatechin gallate following 3-nitropropionic acid-induced brain damage: possible nitric oxide mechanisms

Abstract

The present study shows that EGCG attenuate 3-NP-induced neurotoxicity, and nitric oxide modulation might be involved in its protective action.

Protopanaxtriol protects against 3-nitropropionic acid-induced oxidative stress in a rat model of Huntington's disease

“…Antioxidative drugs [20] and the overexpression of genes involved in attenuating oxidative stress showed significant neuroprotective effects against 3-NP-mediated neurotoxicity [11,31] . Ppt warrants attention as a potential anti-oxidative therapy for HD.…”

“…Intriguingly, systemic treatment with Ppt for 5 days restored the weight loss and mitigated the behavior disorders in the 3-NP treated rats. Kumar et al have shown that antioxidative treatments restore behavioral disorders and antioxidative defense mechanisms in 3-NP treated animals [10,11,31] . In the CNS, cells are able to defend against oxidative stress using several resources, including vitamins, bioactive molecules, lipoic acid, enzymes (such as SOD, GSH, GPx, HO-1, and NQO1), and redox sensitive protein transcription factors (such as AP-1, Nrf2, and HSF) [32,33] .…”

“…Mitochondrial respiratory chain complexes that produce ATP for cellular functioning can be damaged by 3-NP-induced neurotoxicity both in vivo and in vitro [11] . NAC is a classic antioxidant, and it has been reported that NAC increases complex I, II, and IV activities, both in vitro and in vivo in synaptic mitochondrion preparations from aged mice [34] .…”

“…In the present study, we used 3-nitropropionic acid (3-NP), a toxin produced by a number of fungal and plant species, as the model agent mimicking the characteristics of HD [5,6] . 3-NP is an irreversible inhibitor www.nature.com/aps Gao Y et al Acta Pharmacologica Sinica npg of mitochondrial succinate dehydrogenase (SDH), which has been used to explore the molecular mechanisms of cell death associated with mitochondrial dysfunction and neurodegeneration, such as in HD [7,8] ; 3-NP can significantly induce oxidative damage and impair antioxidant defense enzymes in the brain [9][10][11][12][13][14][15][16] . It has also been reported that systemic 3-NP administration leads to oxidized proteins in the striatum, as well as a massive loss of striatal neurons [16] .…”

“…It has also been reported that systemic 3-NP administration leads to oxidized proteins in the striatum, as well as a massive loss of striatal neurons [16] . These lesions may involve secondary excitotoxic oxidative stress and ATP failure mechanisms [11] . Although HD may arise through several mechanisms, there is much evidence for the role of oxidative stress in the development of HD [17] .…”