Mulberry fruit improves memory in scopolamine-treated mice: role of cholinergic function, antioxidant system, and TrkB/Akt signaling.
Suk Kyung ShinJae-Myung YooFu Yi LiSeong Yeon BaekMee Ree KimPublished in: Nutritional neuroscience (2019)
Objectives: Although mulberry fruit possesses some biological activities, it is not known how it protects neuronal cells in neurodegenerative diseases. Here, we examined whether mulberry fruit extract (MFE) protected neuronal cells against oxidative stress-induced neurodegeneration.Methods: In this experiments, glutamate challenged hippocampal neuronal HT-22 cell lines as an in vitro model and scopolamine-induced memoty-impairment mice model were used.Results: MFE improved cell viability and glutathione level as well as reducing reactive oxygen species level in glutamate-treated HT-22 cells. Additionally, MFE suppressed apoptotic bodies and mitochondrial depolarization through regulating expression of apoptosis-related proteins. Furthermore, MFE elevated expression of p-TrkB, p-Akt, p-CREB, BDNF, and antioxidant enzymes as well as nuclear translocation of Nrf2. In contrast, the inclusion of K252a, a TrkB inhibitor, or MK-2206, an Akt selective inhibitor, neutralized the neuroprotective actions of MFE. Separately, MFE attenuated scopolamine-induced amnesia via regulating the activities of enzymes related with cholinergic function and the antioxidant system in mice. Additionally, MFE protected neuronal cells in the hippocampal CA1 and CA3 regions in brain of mice.Conclusions: MFE protects neuronal cells against oxidative stress-induced apoptosis through upregulating the expression of BDNF and antioxidant enzymes by stabilizing the activation of the TrkB/Akt pathway. Such an effect of MFE, which includes rich polyphenols, may provide information for its application as a food supplement for the prevention and treatment of neurodegenerative diseases.
Keyphrases
- induced apoptosis
- oxidative stress
- signaling pathway
- endoplasmic reticulum stress
- diabetic rats
- cell cycle arrest
- cerebral ischemia
- cell death
- ischemia reperfusion injury
- dna damage
- cell proliferation
- poor prognosis
- pi k akt
- reactive oxygen species
- anti inflammatory
- healthcare
- type diabetes
- multiple sclerosis
- high fat diet induced
- adipose tissue
- magnetic resonance
- drug induced
- risk assessment
- computed tomography
- blood brain barrier
- protein kinase
- human health
- health information
- insulin resistance
- smoking cessation
- white matter
- heat shock protein
- stress induced