Neuroprotective effects of grape seed extract on neuronal injury by inhibiting DNA damage in the gerbil hippocampus after transient forebrain ischemia

Hwang, In Koo; Yoo, Ki‐Yeon; Kim, Duk Soo; Jeong, Youn-Kab; Kim, Jong Dai; Shin, Hyun‐Kyung; Lim, Soon Sung; Yoo, Ick Dong; Kang, Tae‐Cheon; Kim, Dongwoo; Moon, Won-Kuk; Won, Moo Ho

doi:10.1016/j.lfs.2004.05.013

Cited by 64 publications

(47 citation statements)

References 33 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…To assess oxidative DNA damage after ischemia with or without HGF treatment, we measured 8-OHdG as an indicator of oxidative DNA damage, as its expression is elevated after oxidative DNA damage (Pastoriza Gallego and Sarasin, 2003;Toyokuni et al, 1997). In fact, the expression of 8-OHdG was shown earlier to be increased after transient forebrain ischemia (Won et al, 2001;Hwang et al, 2004;Baek et al, 2000). In agreement with these findings, we showed that the expression of 8-OHdG was elevated at the early period after the start of reperfusion.…”

Section: Discussionsupporting

confidence: 90%

Prevention of Apoptosis-Inducing Factor Translocation is a Possible Mechanism for Protective Effects of Hepatocyte Growth Factor against Neuronal Cell Death in the Hippocampus after Transient Forebrain Ischemia

Niimura

Takagi

et al. 2006

J Cereb Blood Flow Metab

View full text Add to dashboard Cite

Hepatocyte growth factor (HGF) is one of the prospective agents for therapy against a variety of neurologic and neurodegenerative disorders, although the precise mechanisms for the effect of HGF remain to be elucidated. We showed that treatment with HGF protected hippocampal cornu ammonis (CA) subregion 1 neurons from apoptotic cell death after transient forebrain ischemia. Accumulating evidence indicates that ischemia-induced neuronal damage occurs via caspase-independent pathways. In the present study, we focused on the localization of apoptosis-inducing factor (AIF), which is an important protein in the signal-transduction system through caspase-independent pathways, to investigate the possible mechanism for the protective effect of HGF after transient forebrain ischemia. Hepatocyte growth factor attenuated the increase in the expression of AIF protein in the nucleus after transient forebrain ischemia. We further explored the upstream components of AIF translocation. Primary DNA damage induced by Ca 2 + influx and subsequent NO formation are thought to be the initial events for AIF translocation, which results in the subsequent DNA damage by AIF. Hepatocyte growth factor prevented the primary oxidative DNA damage, as was estimated by using anti-8-OHdG (8-hydroxy-2 0 -deoxyguanosine) antibody. Oxidative DNA damage after ischemia is known to lead to the activation of poly(ADP-ribose) polymerase (PARP) and p53, resulting in AIF translocation. Marked increases in the PAR polymer formation and the expression of p53 protein after ischemia were effectively prevented by HGF treatment. In the present study, we first showed that HGF was capable of preventing neuronal cell death by inhibiting the primary oxidative DNA damage and then preventing the activation of the PARP/p53/AIF pathway.

show abstract

Section: Discussionsupporting

confidence: 90%

Prevention of Apoptosis-Inducing Factor Translocation is a Possible Mechanism for Protective Effects of Hepatocyte Growth Factor against Neuronal Cell Death in the Hippocampus after Transient Forebrain Ischemia

Niimura

Takagi

et al. 2006

J Cereb Blood Flow Metab

View full text Add to dashboard Cite

show abstract

“…The seeds were identified and authenticated by professor J. D. Kim, and a voucher specimen was deposited at the Regional Innovation Center, Hallym University, Chuncheon, Korea. The method of preparation of EAKS was reported previously by Hwang et al (2004). In brief, for the preparation of the ethanol EAKS, Alpinia katsumadai seeds were washed with distilled water and air-dried at 60°C and ground into fine powder.…”

Section: Preparation Of Eaksmentioning

confidence: 99%

Neuroprotective effects ofAlpinia katsumadaiagainst experimental ischemic damage via control of oxidative stress

Park

Lee

et al. 2012

Pharmaceutical Biology

Self Cite

View full text Add to dashboard Cite

show abstract

“…Catechins and epicatechins in cranberry juice and chocolate have anti-oxidant activities, induce apoptosis in cancer cells, inhibit bacterial growth in urinary tract infections, and reduce atherosclerosis (Aruoma et al, 2006). Lastly, grape seed extracts rich in proanthocyanidins are effective antioxidants and may promote cardiac recovery after ischemia (Hwang et al, 2004).…”

Section: Isoflavones: Synthesis Function and Soymentioning

confidence: 99%

Nature’s assembly line: biosynthesis of simple phenylpropanoids and polyketides

Yu¹,

Jez

2008

The Plant Journal

151

View full text Add to dashboard Cite

SummaryPlants produce large amounts of phenylpropanoids, both in terms of molecular diversity and absolute quantity of these compounds. The phenylpropanoids, and the related plant polyketides, have multiple biological functions. They serve to attract pollinators, support secondary cell-wall growth, provide protection against various plant diseases, and interact with beneficial soil microbes. Their basic chemical properties also make them useful in the biofuel and biomaterial industries. Phenylpropanoid metabolism begins with the amino acid phenylalanine, which feeds into various biosynthetic pathways that generate a wide range of structurally related polyphenolic compounds. This review focuses on four sub-groups of these polyphenolic compoundspolyketides, stilbenes, isoflavones and catechins. We discuss the biosynthesis of these molecules, their physiological role in plants, and their striking pharmacological and physiological effects on humans. This review also highlights metabolic engineering efforts aimed at increasing or decreasing the amounts of each class of compound in various model plants and crops.

show abstract

Neuroprotective effects of grape seed extract on neuronal injury by inhibiting DNA damage in the gerbil hippocampus after transient forebrain ischemia

Cited by 64 publications

References 33 publications

Prevention of Apoptosis-Inducing Factor Translocation is a Possible Mechanism for Protective Effects of Hepatocyte Growth Factor against Neuronal Cell Death in the Hippocampus after Transient Forebrain Ischemia

Prevention of Apoptosis-Inducing Factor Translocation is a Possible Mechanism for Protective Effects of Hepatocyte Growth Factor against Neuronal Cell Death in the Hippocampus after Transient Forebrain Ischemia

Neuroprotective effects ofAlpinia katsumadaiagainst experimental ischemic damage via control of oxidative stress

Nature’s assembly line: biosynthesis of simple phenylpropanoids and polyketides

Contact Info

Product

Resources

About