Moringa seed extract alleviates titanium oxide nanoparticles (TiO2-NPs)-induced cerebral oxidative damage, and increases cerebral mitochondrial viability

To investigate the influence of Moringa seed extract (MSE) on the cerebral Nrf2/NQO1 signaling in TiO 2 -NPs–induced brain damage, 80 male albino rats were divided into four groups ( n  = 20); group I was used as a control, group II received TiO 2 -NPs (500 mg/kg b.w/day orally) for 14 days, group I...

Ausführliche Beschreibung

Gespeichert in:
Bibliographische Detailangaben
Veröffentlicht in:Environmental science and pollution research international 2020-06, Vol.27 (16), p.19169-19184
Hauptverfasser: Kandeil, Mohamed A., Mohammed, Eman T., Hashem, Khalid S., Aleya, Lotfi, Abdel-Daim, Mohamed M.
Format: Artikel
Sprache:eng
Schlagworte:
Online-Zugang:Volltext
Tags: Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
Beschreibung
Zusammenfassung:To investigate the influence of Moringa seed extract (MSE) on the cerebral Nrf2/NQO1 signaling in TiO 2 -NPs–induced brain damage, 80 male albino rats were divided into four groups ( n  = 20); group I was used as a control, group II received TiO 2 -NPs (500 mg/kg b.w/day orally) for 14 days, group III received MSE (100 mg/kg b.w/day orally) for 30 days, and group IV received MSE an hour before TiO 2 -NPs administration with the same doses as before. Administration of TiO 2 -NPs was started on the 17th day for both groups (II) and (IV). Administration of MSE significantly increased the cerebral mitochondrial viability and Nrf2 level with a simultaneous increase of NQO1 mRNA expression. This designates a powerful antioxidant effect of MSE which is indicated by a significant reduction of INOS expression, MDA, TOS, OSI levels, and DNA fragmentation % with a significant increase of GSH concentration, SOD activities, and TAC. MSE possesses an anti-inflammatory effect by a significant reduction of IL-1β and TNF-α levels, and anti-apoptotic effect manifested by a significant reduction of caspase-3 and Fas levels. In harmonization, dopamine, serotonin concentrations, and acetylcholinesterase activities return back to normal as compared to control group. These results were confirmed by the histopathological features which were alleviated with MSE administration. In conclusion, Nrf2 plays a pivotal role in the mechanism of TiO 2 -NPs cerebral toxicity and MSE as a Nrf2 activator can provide a powerful cerebroprotective effect, whereas MSE increased the Nrf2 expression and consequently restore the antioxidant activity of brain cells by increasing NQO1 gene expression and cerebral mitochondrial viability as well as inhibition of pro-inflammatory and apoptotic mediators.
ISSN:0944-1344
1614-7499
DOI:10.1007/s11356-019-05514-2