Prospective role of mitochondrial apoptotic pathway in mediating GMG-ITC to reduce cytotoxicity in H2O2-induced oxidative stress in differentiated SH-SY5Y cells - 01/10/19
, Norshariza Nordin c , Rozita Rosli c, d , Khozirah Shaari e, f , Hauwa’u Yakubu Bako b , Noramaliza Mohd Noor g , Ahmad Faizal Abdull Razis a, h, i, ⁎ Bienvenue sur EM-consulte, la référence des professionnels de santé.
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| pages | 12 |
| Iconographies | 7 |
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Highlights |
• | Glucomoringin was isolated, characterised and activated into isothiocyanate. |
• | Seven days retinoic acid treatment robustly influenced neuronal differentiation of SH-SY5Y. |
• | GMG-ITC abrogated the production of ROS and enhanced neuronal cell viability. |
• | GMG-ITC confer prospective neuroprotective ability through mitochondrial signalling pathway. |
Abstract |
The antioxidant and neuroprotective activity of Glucomoringin isothiocyanate (GMG-ITC) have been reported in in vivo and in vitro models of neurodegenerative diseases. However, its neuroprotective role via mitochondrial-dependent pathway in a noxious environment remains unknown. The main objective of the present study was to unveil the mitochondrial apoptotic genes’ profile and prospectively link with neuroprotective activity of GMG-ITC through its ROS scavenging. The results showed that pre-treatment of differentiated SH-SY5Y cells with 1.25 μg/mL purified isolated GMG-ITC, significantly reduced reactive oxygen species (ROS) production level, compared to H2O2 control group, as evidenced by flow cytometry-based evaluation of ROS generation. Presence of GMG-ITC prior to development of oxidative stress condition, downregulated the expression of cyt-c, p53, Apaf-1, Bax, CASP3, CASP8 and CASP9 genes with concurrent upregulation of Bcl-2 gene in mitochondrial apoptotic signalling pathway. Protein Multiplex revealed significant decreased in cyt-c, p53, Apaf-1, Bax, CASP8 and CASP9 due to GMG-ITC pre-treatment in oxidative stress condition. The present findings speculated that pre-treatment with GMG-ITC may alleviate oxidative stress condition in neuronal cells by reducing ROS production level and protect the cells against apoptosis via neurodegenerative disease potential pathways.
Le texte complet de cet article est disponible en PDF.Abbreviations : AD, ALS, Apaf-1, ARE, ATRA, Bax, BCA, Bcl-2, Bim, BSA, CASP, cyt-c, DMEM/F12, DMSO, EDTA, EMC7, ESI, FBS, FITC, GMG-ITC, GPI, HD, H2O2, KanR, Mcl-1, MFI, MPTP, MYR, MTT, NCBI, NDD, Nrf2, OligoCalc, p53, PBS, PCR, PD, PSMB4, RIN, RIPA, RNA, ROS, RPM, RT, SAPE, SD, SCI, SH-SY5Y, SNRPD3, SPSS, Taq, Tuj-1, UMBI, UPM, XP
Keywords : Apoptosis, Glucomoringin-isothiocyanate, Mitochondria, Neurodegenerative diseases, Neuroprotection, Oxidative stress
Plan
Vol 119
Article 109445- novembre 2019 Retour au numéro
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