Green tea polyphenols inhibit cognitive impairment induced by chronic cerebral hypoperfusion via modulating oxidative stress

2010 ◽  
Vol 21 (8) ◽  
pp. 741-748 ◽  
Author(s):  
Yan Xu ◽  
Jun-jian Zhang ◽  
Li Xiong ◽  
Lei Zhang ◽  
Dong Sun ◽  
...  
2019 ◽  
Vol 73 ◽  
pp. 108213 ◽  
Author(s):  
Yuting Song ◽  
Xiuxiu Li ◽  
Xiangdan Gong ◽  
Xin Zhao ◽  
Zhengliang Ma ◽  
...  

Circulation ◽  
2014 ◽  
Vol 130 (suppl_2) ◽  
Author(s):  
Tzu -Hsien Tsai ◽  
Sarah Chua ◽  
Jiunn-Jye Sheu ◽  
Steve Leu ◽  
Hon Kan Yip

Background: Sitagliptin, a new anti-diabetic drug that inhibits dipeptidyl peptidase (DPP)-4 enzyme activity, has been reported to possess neuroprotective property. We tested the protective effect of sitagliptin against chronic cerebral hypoperfusion (CHP) in mice after bilateral carotid artery stenosis (BCAS). Methods: Thirty C57BL/6 mice were divided into three groups: Sham control (SC) (n=10), CHP (n=10), CHP-sitagliptin (orally 600mg/kg/day) (n=10). Working memory was assessed with novel-object recognition test. Magnetic resonance imaging (MRI) was performed at day 0 and day 90 after BCAS procedure prior to sacrifice. Results: Immunohistochemical (IHC) staining showed significantly enhanced microglia activation, astrocytosis, and demyelinating change of white matter in CHP group than in SC but the changes were significantly suppressed after sitagliptin treatment (all p<0.01). The mRNA expressions of inflammatory (TNF-α, MCP-1and MMP-2) and apoptotic (Bax) biomarkers showed an identical pattern, whereas the anti-inflammatory (IL-10) and anti-apoptotic (Bcl-2) biomarkers showed an opposite pattern compared to that of IHC among all groups (all p<0.01). The protein expressions of oxidative stress (NOX-I, NOX-II, nitrotyrosin, oxidized protein), inflammatory (NF-κB, TNF-α and MMP-2), apoptotic (mitochondrial Bax, cleaved PARP), and DNA-damage (γ-H2AX) markers showed an identical pattern, while expression pattern of anti-apoptotic marker (Bcl-2) was opposite to that of IHC (all p<0.01). Glycogen-like peptide-1 receptor protein expression progressively increased from SC to CHP-sitagliptin (p<0.01). The short-term working-memory loss and cortical-matter reduction on MRI-T2 showed a pattern identical to that of IHC in all groups (all p<0.01). Conclusion: Sitagliptin protected against cognitive impairment and brain damage in a murine CHP model. Key words: chronic cerebral hypoperfusion, sitagliptin, oxidative stress inflammation


2008 ◽  
Vol 24 (5) ◽  
pp. 305-313 ◽  
Author(s):  
Zhi-You Cai ◽  
Yong Yan ◽  
Shan-Quan Sun ◽  
Jun Zhang ◽  
Liang-Guo HUANG ◽  
...  

2012 ◽  
Vol 2012 ◽  
pp. 1-12 ◽  
Author(s):  
Takako Yokozawa ◽  
Jeong Sook Noh ◽  
Chan Hum Park

Green tea, prepared from the leaves ofCamellia sinensisL., is a beverage that is popular worldwide. Polyphenols in green tea have been receiving much attention as potential compounds for the maintenance of human health due to their varied biological activity and low toxicity. In particular, the contribution of antioxidant activity to the prevention of diseases caused by oxidative stress has been focused upon. Therefore, in this study, we investigated the effects of (−)-epigallocatechin 3-O-gallate and (−)-epigallocatechin 3-O-gallate, which account for a large fraction of the components of green tea polyphenol, on oxidative stress-related renal disease. Our observations suggest that green tea polyphenols have a beneficial effect on pathological states related to oxidative stress of the kidney.


2006 ◽  
Vol 73 (2) ◽  
pp. 572-580 ◽  
Author(s):  
Kazuhiro Maeta ◽  
Wataru Nomura ◽  
Yoshifumi Takatsume ◽  
Shingo Izawa ◽  
Yoshiharu Inoue

ABSTRACT Epigallocatechin gallate (EGCG) is the most abundant polyphenolic flavonoid in green tea. Catechin and its derivatives, including EGCG, are widely believed to function as antioxidants. Here we demonstrate that both EGCG and green tea extract (GTE) cause oxidative stress-related responses in the budding yeast Saccharomyces cerevisiae and the fission yeast Schizosaccharomyces pombe under weak alkaline conditions in terms of the activation of oxidative-stress-responsive transcription factors. GTE as well as EGCG induced the nuclear localization of Yap1 in S. cerevisiae, which was repressed by the addition of catalase but not by the addition of superoxide dismutase. The same phenomena were observed for the nucleocytoplasmic localization of Msn2 in S. cerevisiae and Pap1, a Yap1 homologue, in S. pombe. The formation of intramolecular disulfide bonds has been proposed to be crucial for the H2O2-induced nuclear localization of Yap1, and we verified the importance of cysteine residues of Yap1 in response to EGCG and GTE. Additionally, we show that EGCG and GTE produce H2O2 in a weak alkaline medium. Finally, we conclude that tea polyphenols are able to act as prooxidants to cause a response to oxidative stress in yeasts under certain conditions.


2017 ◽  
Vol 2017 ◽  
pp. 1-14 ◽  
Author(s):  
Weijie Yi ◽  
Xiao Xie ◽  
Miying Du ◽  
Yongjun Bu ◽  
Nannan Wu ◽  
...  

Scope. Several reports in the literature have suggested the renoprotective effects of ketone bodies and green tea polyphenols (GTPs). Our previous study found that GTP consumption could elevate the renal expression of the ketogenic rate-limiting enzyme, which was decreased by a high-fat diet (HFD) in rats. Here, we investigated whether ketogenesis can mediate renoprotection by GTPs against an HFD. Methods and Results. Wistar rats were fed a standard or HFD with or without GTPs for 18 weeks. The renal oxidative stress level, kidney function, renal expression, and activity levels of mitochondrial 3-hydroxy-3-methylglutaryl-CoA (HMG-CoA) synthase 2 (HMGCS2) and sirtuin 3(SIRT3) were detected. The increased renal oxidative stress and the loss of renal function induced by the HFD were ameliorated by GTPs. Renal ketogenesis and SIRT3 expression and activity levels, which were reduced by the HFD, were restored by GTPs. In vitro, HEK293 cells were transfected with the eukaryotic expression plasmid pcDNA HMGCS2. GTP treatment could upregulate HMGCS2 and SIRT3 expression. Although SIRT3 expression was not affected by HMGCS2 transfection, the 4-hydroxy-2-nonenal (4-HNE) level and the acetyl-MnSOD (K122)/MnSOD ratio were reduced in HMGCS2-transfected cells in the context of H2O2. Conclusion. The ketogenesis/SIRT3 pathway mediates the renoprotection of GTPs against the oxidative stress induced by an HFD.


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