3,3'-Diindolylmethane Promotes BDNF and Antioxidant Enzyme Formation via TrkB/Akt Pathway Activation for Neuroprotection against Oxidative Stress-Induced Apoptosis in Hippocampal Neuronal Cells.

Autor:	Lee BD; Department of Food and Nutrition, Chungnam National University, Daejeon 34134, Korea., Yoo JM; Korean Medicine-Application Center, Korea Institute of Oriental Medicine, Daegu 41062, Korea.; Korean Medicine R&D Team 1, National Institute for Korean Medicine Development, Gyeongsan 38540, Korea., Baek SY; Department of Food and Nutrition, Chungnam National University, Daejeon 34134, Korea., Li FY; Department of Food and Nutrition, Chungnam National University, Daejeon 34134, Korea., Sok DE; College of Pharmacy, Chungnam National University, Daejeon 34134, Korea., Kim MR; Department of Food and Nutrition, Chungnam National University, Daejeon 34134, Korea.
Jazyk:	angličtina
Zdroj:	Antioxidants (Basel, Switzerland) [Antioxidants (Basel)] 2019 Dec 18; Vol. 9 (1). Date of Electronic Publication: 2019 Dec 18.
DOI:	10.3390/antiox9010003
Abstrakt:	3,3'-Diindolylmethane (DIM), a metabolite of indole-3-carbinol present in Brassicaceae vegetables, possesses various health-promoting effects. Nonetheless, the effect of DIM on neurodegenerative diseases has not been elucidated clearly. In this study, we hypothesized DIM may protect neuronal cells against oxidative stress-induced apoptosis by promoting the formation of brain-derived neurotrophic factor (BDNF) and antioxidant enzymes through stabilizing the activation of the tropomyosin-related kinase receptor B (TrkB) cascade and we investigated the effect of DIM on oxidative stress-mediated neurodegenerative models. DIM protected neuronal cells against oxidative stress-induced apoptosis by regulating the expression of apoptosis-related proteins in glutamate-treated HT-22 cells. Additionally, DIM improved the expression of BDNF and antioxidant enzymes, such as heme oxygenase-1, glutamate-cysteine ligase catalytic subunit, and NAD(P)H quinine oxidoreductase-1, by promoting the activation of the TrkB/protein kinase B (Akt) pathway in the cells. Consistent with in vitro studies, DIM attenuated memory impairment by protecting hippocampal neuronal cells against oxidative damage in scopolamine-treated mice. Conclusionally, DIM exerted neuroprotective and antioxidant actions through the activation of both BDNF production and antioxidant enzyme formation in accordance with the TrkB/Akt pathway in neuronal cells. Such an effect of DIM may provide information for the application of DIM in the prevention of and therapy for neurodegenerative diseases. Competing Interests: The authors declare no conflict of interest.
Databáze:	MEDLINE
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