Dépôt numérique

Bacopa monniera extract protects against oxidative stress and mitochondrial dysfunctions induced my MPP+, rotenone and H202.

Singh, Manjeet; Ramassamy, Charles . Bacopa monniera extract protects against oxidative stress and mitochondrial dysfunctions induced my MPP+, rotenone and H202. In: Congrès Armand-Frappier 2009, 6e édition, 5-7 novembre 2009, Bromont.

PDF - Version publiée
Télécharger (153kB) | Prévisualisation


Parkinson’s disease (PD) is one of the most common forms of neurodegenerative diseases affecting millions of people worldwide. Oxidative stress (OS) and mitochondrial dysfunctions play an important role in the pathophysiology and progression of PD. Recently natural antioxidants from fruits, vegetable and herbs have shown neuroprotection both in vitro and in vivo models of PD. Here we present our data on the neuroprotective activity of one of the Indian medicinal plants i.e. Bacopa monniera (BM) on SK-N-SH cells. We investigated the neuroprotective effects of BM against 1-methyl-4-phenyl-pyridinium (MPP+), rotenone and hydrogen peroxide (H2O2) - induced toxicity. MPP+ and rotenone are widely used toxins in vitro and in animal models of PD. Using cell survival assay, XTT test our results demonstrated that the BM extract can protect SKN- SH cells against H2O2 (50 μM), Rotenone (1.0μM) or MPP+ (0.5mM)-induced toxicity. These protections were completed with the toxicity test LDH. MPP+ is known to induce cell toxicity by disrupting the mitochondrial activity. Therefore, we have investigated the effect of BM on the mitochondrial membrane potential (MMP) with the JC1. We found that the BM extract significantly protected against the MPP+-induced loss of MMP. Our results also show that the BM extract could also prevent the opening of mitochondrial permeability pore. BM extract also activated Sirt1, HO-1, p-AKT, pERK1/2 and Nrf2 pathways which are regulated by OS and have been implicated in PD. In conclusion, our data suggest that the BM extract can protect neurons against MPP+, Rotenone and H2O2- induced neurotoxicity through different mechanisms, by decreasing OS, preserving mitochondrial functions and by regulating the activities of redox sensitive pathways. Further ongoing studies are likely to elucidate additional mechanisms involved in the neuroprotection and its application in the prevention of PD.

Type de document: Document issu d'une conférence ou d'un atelier
Informations complémentaires: Affiche scientifique
Mots-clés libres: -
Centre: Centre INRS-Institut Armand Frappier
Date de dépôt: 16 sept. 2017 00:49
Dernière modification: 16 sept. 2017 00:49
URI: http://espace.inrs.ca/id/eprint/6100

Actions (Identification requise)

Modifier la notice Modifier la notice