Protective effects of a green tea polyphenol, epigallocatechin-3-gallate, against sevoflurane-induced neuronal apoptosis involve regulation of CREB/BDNF/TrkB and PI3K/Akt/mTOR signalling pathways in neonatal mice

2017 ◽  
Vol 95 (12) ◽  
pp. 1396-1405 ◽  
Author(s):  
Mei-li Ding ◽  
Hui Ma ◽  
Yi-gang Man ◽  
Hong-yan LV
Keyword(s):  
Learning And Memory ◽  
Green Tea ◽  
Survivin Expression ◽  
Terminal Deoxynucleotidyl Transferase ◽  
Mrna Levels ◽  
Protective Effects ◽  
Neonatal Mice ◽  
Fluoro Jade B ◽  
Green Tea Polyphenol ◽  
Gsk 3Β

Epigallocatechin-3-gallate (EGCG), a polyphenol in green tea, is an effective antioxidant and possesses neuroprotective effects. Brain-derived neurotrophic factor (BDNF) and cyclic AMP response element-binding protein (CREB) are crucial for neurogenesis and synaptic plasticity. In this study, we aimed to assess the protective effects of EGCG against sevoflurane-induced neurotoxicity in neonatal mice. Distinct groups of C57BL/6 mice were given EGCG (25, 50, or 75 mg/kg body weight) from postnatal day 3 (P3) to P21 and were subjected to sevoflurane (3%; 6 h) exposure on P7. EGCG significantly inhibited sevoflurane-induced neuroapoptosis as determined by Fluoro-Jade B staining and terminal deoxynucleotidyl transferase dUTP nick end labelling (TUNEL). Increased levels of cleaved caspase-3, downregulated Bad and Bax, and significantly enhanced Bcl-2, Bcl-xL, xIAP, c-IAP-1, and survivin expression were observed. EGCG induced activation of the PI3K/Akt pathway as evidenced by increased Akt, phospho-Akt, GSK-3β, phospho-GSK-3β, and mTORc1 levels. Sevoflurane-mediated downregulation of cAMP/CREB and BDNF/TrkB signalling was inhibited by EGCG. Reverse transcription PCR analysis revealed enhanced BDNF and TrkB mRNA levels upon EGCG administration. Improved performance of mice in Morris water maze tests suggested enhanced learning and memory. The study indicates that EGCG was able to effectively inhibit sevoflurane-induced neurodegeneration and improve learning and memory retention of mice via activation of CREB/BDNF/TrkB–PI3K/Akt signalling.

scholarly journals Heat Acclimation Regulates the Autophagy-Lysosome Function to Protect Against Heat Stroke-Induced Brain Injury in Mice

2017 ◽  
Vol 41 (1) ◽  
pp. 101-114 ◽  
Author(s):  
Junfeng Yi ◽  
Genlin He ◽  
Ju Yang ◽  
Zhen Luo ◽  
Xuesen Yang ◽  
...  
Keyword(s):  
Brain Injury ◽  
Neuroprotective Effect ◽  
Heat Stroke ◽  
Microscopic Analysis ◽  
Heat Acclimation ◽  
Terminal Deoxynucleotidyl Transferase ◽  
Autophagic Flux ◽  
Protective Effects ◽  
Electron Microscopic ◽  
Fluoro Jade B

Background/Aims: The mechanisms underlying the protective role of heat acclimation (HA) in heat stroke (HS)-induced brain injury are still unclear. The autophagy-lysosome pathway is known to pay an important role in protecting stressed or diseased cells from death. Nevertheless, whether autophagy and lysosomes are involved in HA-mediated neuroprotection following HS exposure remains unclear. Methods: The protective effects of HA were assessed by rectal temperature, hematoxylin-eosin staining, transmission electron microscopic analysis, terminal deoxynucleotidyl transferase-mediated dUTP nick end-labeling staining, and Fluoro Jade B staining, after mice were subjected to HS. The effects of HA on autophagy and lysosomes were assessed in the presence of the autophagy inhibitor 3-methyladenine (3MA). Autophagy and lysosome-associated proteins were analysed by Western blotting. Results: We found that HA protected against HS-induced death and brain injury. HS can robustly induce autophagy and impair lysosome function. HA pre-conditioning significantly modulated the autophagy level, and improved lysosome function in HS mice. Furthermore, 3MA completely abolished the neuroprotective effect of HA on HS. Conclusion: HS may induce brain injury through lysosomal dysfunction and impaired autophagic flux. HA protected against HS-induced brain injury via a mechanism involving the autophagy-lysosome pathway.

scholarly journals Protective Effects of Green Tea Polyphenol Against Renal Injury Through ROS-Mediated JNK-MAPK Pathway in Lead Exposed Rats

2016 ◽  
Vol 39 (6) ◽  
pp. 508-513 ◽  
Author(s):  
Haidong Wang ◽  
Deyuan Li ◽  
Zhongze Hu ◽  
Siming Zhao ◽  
Zhejun Zheng ◽  
...  
Keyword(s):  
Green Tea ◽  
Renal Injury ◽  
Mapk Pathway ◽  
Protective Effects ◽  
Tea Polyphenol ◽  
Green Tea Polyphenol

scholarly journals Green tea polyphenol EGCG suppresses Wnt/β-catenin signaling by promoting GSK-3β- and PP2A-independent β-catenin phosphorylation/degradation

BioFactors ◽  
2014 ◽  
Vol 40 (6) ◽  
pp. 586-595 ◽  
Author(s):  
Sangtaek Oh ◽  
Jungsug Gwak ◽  
Seoyoung Park ◽  
Chung S. Yang
Keyword(s):  
Green Tea ◽  
Tea Polyphenol ◽  
Green Tea Polyphenol ◽  
Gsk 3Β

scholarly journals Protective effects of green tea polyphenol against cisplatin-induced nephrotoxicity in rats

2014 ◽  
Vol 57 (6) ◽  
pp. 464 ◽  
Author(s):  
Tae-Gyu Ahn ◽  
Han-Kyoung Kim ◽  
So-Won Park ◽  
Soo-Ah Kim ◽  
Byoung-Rai Lee ◽  
...  
Keyword(s):  
Green Tea ◽  
Protective Effects ◽  
Tea Polyphenol ◽  
Green Tea Polyphenol

Protective Effects of Green Tea Seed Extract against UVB-irradiated Human Skin Fibroblasts

2014 ◽  
Vol 43 (1) ◽  
pp. 1-8 ◽  
Author(s):  
Ok Kyung Kim ◽  
Da-Eun Nam ◽  
Min-Jae Lee ◽  
Namgil Kang ◽  
Jae-Youn Lim ◽  
...  
Keyword(s):  
Human Skin ◽  
Green Tea ◽  
Seed Extract ◽  
Skin Fibroblasts ◽  
Protective Effects ◽  
Human Skin Fibroblasts

The Protective Effects of Green Tea Catechins in the Management of Neurodegenerative Diseases: A Review

2019 ◽  
Vol 16 (1) ◽  
pp. 57-65 ◽  
Author(s):  
Tahereh Farkhondeh ◽  
Hanieh Shaterzadeh Yazdi ◽  
Saeed Samarghandian
Keyword(s):  
Neurodegenerative Diseases ◽  
Signaling Pathways ◽  
Green Tea ◽  
Molecular Mechanisms ◽  
Main Role ◽  
Related Factor ◽  
Protective Effects ◽  
Tea Catechins ◽  
Green Tea Catechins ◽  
And Control

Background: The therapeutic strategies to manage neurodegenerative diseases remain limited and it is necessary to discover new agents for their prevention and control. Oxidative stress and inflammation play a main role in the pathogenesis of neurodegenerative diseases. The aim of this study is to review the effects of green tea catechins against the Neurodegenerative Diseases. Methods: In this study, we extensively reviewed all articles on the terms of Green tea, catechins, CNS disorders, and different diseases in PubMed, Science Direct, Scopus, and Google Scholar databases between the years 1990 and 2017. Results: The present study found that catechins, the major flavonoids in green tea, are powerful antioxidants and radical scavengers which possess the potential roles in the management of neurodegenerative diseases. Catechins modulate the cellular and molecular mechanisms through the inflammation-related NF-&amp;#954;B and the nuclear factor erythroid 2-related factor 2 (Nrf2) signaling pathways. Conclusion: The findings of the present review shows catechins could be effective against neurodegenerative diseases due to their antioxidation and anti-inflammation effects and the involved biochemical pathways including Nrf2 and NF-kB signaling pathways.<P&gt;

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