Oleuropein isolated from Fraxinus rhynchophylla inhibits glutamate-induced neuronal cell death by attenuating mitochondrial dysfunction

2017 ◽  
Vol 21 (7) ◽  
pp. 520-528 ◽  
Author(s):  
Mi Hye Kim ◽  
Ju-Sik Min ◽  
Joon Yeop Lee ◽  
Unbin Chae ◽  
Eun-Ju Yang ◽  
...  
2018 ◽  
Vol 2018 ◽  
pp. 1-9 ◽  
Author(s):  
Jade Heejae Ko ◽  
Ju-Hee Lee ◽  
Bobin Choi ◽  
Ju-Yeon Park ◽  
Young-Won Kwon ◽  
...  

Parkinson’s disease is a neurodegenerative disease characterized by progressive cell death of dopaminergic neuron and following neurological disorders. Gagam-Sipjeondaebo-Tang (GST) is a novel herbal formula made of twelve medicinal herbs derived from Sipjeondaebo-Tang, which has been broadly used in a traditional herbal medicine. In the present study, we investigated the effects of GST against 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced motor abnormalities in mice and 1-methyl-4-phenylpyridinium (MPP+)-induced neurotoxicity in SH-SY5Y cell. First, we found that GST alleviated motor dysfunction induced by MPTP, and the result showed dopaminergic neurons recovery in substantia nigra. In the cell experiment, pretreatment with GST increased the cell viability and attenuated apoptotic cell death in MPP+-treated SH-SY5Y cells. GST also inhibited reactive oxygen species production and restored the mitochondrial membrane potential loss, which were induced by MPP+. Furthermore, GST extract significantly activated ERK and Akt, cell survival-related proteins, in SH-SY5Y cells. The effect of GST preventing mitochondrial dysfunction was antagonized by pretreatment of PD98059 and LY294002, selective inhibitors of ERK and Akt, respectively. Taken together, GST alleviated abnormal motor functions and recovered neuronal cell death, mitochondrial dysfunction, possibly via ERK and Akt activation. Therefore, we suggest that GST may be a candidate for the treatment and prevention of Parkinson’s disease.


2000 ◽  
Vol 2 (1) ◽  
pp. 107-107
Author(s):  
L Tranebjaerg ◽  
S Lindal ◽  
S Merchant ◽  
O Ingebretsen ◽  
B Hamel ◽  
...  

2013 ◽  
Vol 36 (3) ◽  
pp. 258-266 ◽  
Author(s):  
Seung-Hoon Baek ◽  
Ok-Nam Bae ◽  
Eun-Kyoung Kim ◽  
Seong-Woon Yu

PLoS ONE ◽  
2009 ◽  
Vol 4 (5) ◽  
pp. e5491 ◽  
Author(s):  
Agnès Petit-Paitel ◽  
Frédéric Brau ◽  
Julie Cazareth ◽  
Joëlle Chabry

Neuron ◽  
2004 ◽  
Vol 41 (3) ◽  
pp. 351-365 ◽  
Author(s):  
Ella Bossy-Wetzel ◽  
Maria V Talantova ◽  
Wilson D Lee ◽  
Marion N Schölzke ◽  
Anne Harrop ◽  
...  

FEBS Letters ◽  
2008 ◽  
Vol 582 (30) ◽  
pp. 4185-4190 ◽  
Author(s):  
Do Yeon Lee ◽  
Kyu-Sun Lee ◽  
Hyun Jung Lee ◽  
Hee-Yeon Jung ◽  
Jun Young Lee ◽  
...  

Atmosphere ◽  
2020 ◽  
Vol 11 (10) ◽  
pp. 1098
Author(s):  
Deborah Cory-Slechta ◽  
Marissa Sobolewski ◽  
Günter Oberdörster

Increasing evidence links air pollution (AP) exposure to effects on the central nervous system structure and function. Particulate matter AP, especially the ultrafine (nanoparticle) components, can carry numerous metal and trace element contaminants that can reach the brain in utero and after birth. Excess brain exposure to either essential or non-essential elements can result in brain dyshomeostasis, which has been implicated in both neurodevelopmental disorders (NDDs; autism spectrum disorder, schizophrenia, and attention deficit hyperactivity disorder) and neurodegenerative diseases (NDGDs; Alzheimer’s disease, Parkinson’s disease, multiple sclerosis, and amyotrophic lateral sclerosis). This review summarizes the current understanding of the extent to which the inhalational or intranasal instillation of metals reproduces in vivo the shared features of NDDs and NDGDs, including enlarged lateral ventricles, alterations in myelination, glutamatergic dysfunction, neuronal cell death, inflammation, microglial activation, oxidative stress, mitochondrial dysfunction, altered social behaviors, cognitive dysfunction, and impulsivity. Although evidence is limited to date, neuronal cell death, oxidative stress, and mitochondrial dysfunction are reproduced by numerous metals. Understanding the specific contribution of metals/trace elements to this neurotoxicity can guide the development of more realistic animal exposure models of human AP exposure and consequently lead to a more meaningful approach to mechanistic studies, potential intervention strategies, and regulatory requirements.


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