Neuroprotective effects of various flavonoids alone and in combination on lipopolysaccharide‐induced neurotoxicity in PC‐12 cells

Abstract Background Hericium erinaceus is a culinary and medicinal mushroom in Traditional Chinese Medicines. It has numerous pharmacological effects including immunomodulatory, anti-tumour, anti-microbial, anti-aging and stimulation of nerve growth factor (NGF) synthesis, but little is known about its potential role in negating the detrimental effects of oxidative stress in depression. The present study investigated the neuroprotective effects of H. erinaceus standardised aqueous extract (HESAE) against high-dose corticosterone-induced oxidative stress in rat pheochromocytoma (PC-12) cells, a cellular model mimicking depression. Methods PC-12 cells was pre-treated with HESAE for 48 h followed by 400 μM corticosterone for 24 h to induce oxidative stress. Cells in complete medium without any treatment or pre-treated with 3.125 μg/mL desipramine served as the negative and positive controls, respectively. The cell viability, lactate dehydrogenase (LDH) release, endogenous antioxidant enzyme activities, aconitase activity, mitochondrial membrane potentials (MMPs), intracellular reactive oxygen species (ROS) levels and number of apoptotic nuclei were quantified. In addition, HESAE ethanol extract was separated into fractions by chromatographic methods prior to spectroscopic analysis. Results We observed that PC-12 cells treated with high-dose corticosterone at 400 μM had decreased cell viability, reduced endogenous antioxidant enzyme activities, disrupted mitochondrial function, and increased oxidative stress and apoptosis. However, pre-treatment with HESAE ranging from 0.25 to 1 mg/mL had increased cell viability, decreased LDH release, enhanced endogenous antioxidant enzyme activities, restored MMP, attenuated intracellular ROS and protected from ROS-mediated apoptosis. The neuroprotective effects could be attributed to significant amounts of adenosine and herierin III isolated from HESAE. Conclusions HESAE demonstrated neuroprotective effects against high-dose corticosterone-induced oxidative stress in an in vitro model mimicking depression. HESAE could be a potential dietary supplement to treat depression.

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The Neuroprotective Effects of Decursin Isolated from Angelica gigas Nakai Against Amyloid β-Protein-Induced Apoptosis in PC 12 Cells via a Mitochondria-Related Caspase Pathway

Neurochemical Research ◽

10.1007/s11064-015-1623-0 ◽

2015 ◽

Vol 40 (8) ◽

pp. 1555-1562 ◽

Cited By ~ 10

Author(s):

Li Li ◽

Jikun Du ◽

Liyi Zou ◽

Haishan Xia ◽

Tie Wu ◽

...

Keyword(s):

Amyloid Β ◽

Amyloid Β Protein ◽

Neuroprotective Effects ◽

Angelica Gigas ◽

Angelica Gigas Nakai ◽

Pc 12 Cells ◽

Β Protein ◽

Caspase Pathway ◽

Induced Apoptosis

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Gems from past: Neuroprotective effects of Bhilawinol and Anacardic acid against Glutamate-induced excitotoxicity in PC-12 cells.

Frontiers in Human Neuroscience ◽

10.3389/conf.fnhum.2019.229.00033 ◽

2019 ◽

Vol 13 ◽

Author(s):

Rukhsana Nawaz ◽

Faisal Khan ◽

Amina Hassan ◽

Nailah Mahmood ◽

Heba Ahmed Naser ◽

...

Keyword(s):

Anacardic Acid ◽

Neuroprotective Effects ◽

Pc 12 Cells

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Apple Procyanidins Suppress Amyloidβ-Protein Aggregation

Biochemistry Research International ◽

10.1155/2011/784698 ◽

2011 ◽

Vol 2011 ◽

pp. 1-8 ◽

Cited By ~ 14

Author(s):

Toshihiko Toda ◽

Tadahiro Sunagawa ◽

Tomomasa Kanda ◽

Motoyuki Tagashira ◽

Takuji Shirasawa ◽

...

Keyword(s):

Alzheimer’S Disease ◽

Alzheimer's Disease ◽

Caenorhabditis Elegans ◽

Protein Aggregation ◽

Protein A ◽

Dependent Manner ◽

Neuroprotective Effects ◽

Pc 12 Cells ◽

The Mean ◽

Dose Dependent

Procyanidins (PCs) are major components of the apple polyphenols (APs). We previously reported that treatment with PC extended the mean lifespan ofCaenorhabditis elegans(Sunagawa et al., 2011). In order to estimate the neuroprotective effects of PC, we investigated the antiaggregative activity of PC on amyloidβ-protein (Aβ) aggregation, which is a pathological hallmark of Alzheimer's disease. We herein report that PC significantly suppressed Aβ42 aggregation and dissociated Aβ42 aggregates in a dose-dependent manner, indicating that PC is a potent suppressor of Aβaggregation. Furthermore, PC significantly inhibited Aβ42 neurotoxicity and stimulated proliferation in PC-12 cells. These results suggested that the PC and AP acted as neuroprotective factors against toxic Aβaggregates.

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Protective effect of chitooligosaccharides on hydrogen peroxide-induced PC-12 cells death by inhibition of oxidative damage

Cell Biology International ◽

10.1042/cbi034s027d ◽

2010 ◽

Vol 34 (8) ◽

pp. S27-S27

Author(s):

Xueling Dai ◽

Ping Chang ◽

Ke Xu ◽

Changjun Lin ◽

Hanchang Huang ◽

...

Keyword(s):

Hydrogen Peroxide ◽

Oxidative Damage ◽

Protective Effect ◽

Pc 12 Cells ◽

Cells Death

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Activity Engagement in Cognitive Aging: A Review of the Evidence

Perspectives on Neurophysiology and Neurogenic Speech and Language Disorders ◽

10.1044/nnsld23.1.35 ◽

2013 ◽

Vol 23 (1) ◽

pp. 1-12 ◽

Cited By ~ 2

Author(s):

Yvonne Rogalski ◽

Muriel Quintana

Keyword(s):

Older Adults ◽

Cognitive Decline ◽

Cognitive Aging ◽

Social Activity ◽

Current Evidence ◽

Omega 3 ◽

Neuroprotective Effects ◽

Activity Engagement ◽

Age Related ◽

Age Related Cognitive Decline

The population of older adults is rapidly increasing, as is the number and type of products and interventions proposed to prevent or reduce the risk of age-related cognitive decline. Advocacy and prevention are part of the American Speech-Language-Hearing Association’s (ASHA’s) scope of practice documents, and speech-language pathologists must have basic awareness of the evidence contributing to healthy cognitive aging. In this article, we provide a brief overview outlining the evidence on activity engagement and its effects on cognition in older adults. We explore the current evidence around the activities of eating and drinking with a discussion on the potential benefits of omega-3 fatty acids, polyphenols, alcohol, and coffee. We investigate the evidence on the hypothesized neuroprotective effects of social activity, the evidence on computerized cognitive training, and the emerging behavioral and neuroimaging evidence on physical activity. We conclude that actively aging using a combination of several strategies may be our best line of defense against cognitive decline.

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