Epigallocatechin-3-gallate, a green tea catechin, protects the heart against regional ischemia–reperfusion injuries through activation of RISK survival pathways in rats

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• 作者：Seok Jai Kim (1)
  Mei Li (2)
  Cheol Won Jeong (3)
  Hong Beom Bae (1)
  Sang Hyun Kwak (1)
  Seong Heon Lee (1)
  Hyun Jung Lee (1)
  Bong Ha Heo (1)
  Keun Bae Yook (1)
  Kyung Yeon Yoo (1)
  
• 关键词：Epigallocatechin ; 3 ; gallate ; Ischemia/reperfusion injury ; RISK pathway ; Pro ; apoptotic pathway
• 刊名：Archives of Pharmacal Research
• 出版年：2014
• 出版时间：August 2014
• 年：2014
• 卷：37
• 期：8
• 页码：1079-1085
• 全文大小：523 KB
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• 作者单位：Seok Jai Kim (1)
  Mei Li (2)
  Cheol Won Jeong (3)
  Hong Beom Bae (1)
  Sang Hyun Kwak (1)
  Seong Heon Lee (1)
  Hyun Jung Lee (1)
  Bong Ha Heo (1)
  Keun Bae Yook (1)
  Kyung Yeon Yoo (1)
  
  1. Department of Anesthesiology and Pain Medicine, Chonnam National University Medical School, 671 Jebong-ro Donggu, Gwangju, 501-57, Korea
  2. Department of Anesthesiology, The First Affiliated Hospital and Zhejiang University Medical School, Hangzhou, Zhejiang, China
  3. Department of Anesthesiology and Pain Medicine, Chonnam National University Dental School, Gwangju, Korea
  
• ISSN：1976-3786

文摘

Epigallocatechin-3-gallate (EGCG), the major catechin derived from green tea, has been shown to modulate numerous molecular targets in the setting of inflammation. This study aimed to determine whether EGCG protects against regional myocardial ischemia/reperfusion (I/R) injuries and its underlying mechanisms involving the role of reperfusion injury salvage kinase (RISK) pathways (PI3K-Akt and ERK 1/2) and GSK-3β or apoptotic kinases (p38 and JNK). The rats were subjected to I/R injuries consisting of 30?min ischemia followed by 2?h reperfusion. EGCG (10?mg/kg, intravenously) was administered alone or along with wortmannin (PI3K inhibitor, 0.6?mg/kg, intravenously) 5?min before the onset of reperfusion. Wortmannin was administered 10?min before the reperfusion. Infarct size was measured at the end of the reperfusion. The phosphorylation of Akt, GSK-3β, and MAPK kinases (ERK1/2, P38 and JNK) was determined by Western blotting after 10?min of reperfusion. EGCG reduced the infarct size compared with the control (25.4?±?9.2 versus 43.2?±?8.2?%, p?Wortmannin alone did not affect the infarct size, but abolished the EGCG-induced infarct size limiting effect, indicating that EGCG may protect the heart by modulating the PI3K-Akt. EGCG significantly enhanced the phosphorylation of Akt and GSK-3β but not ERK1/2, while it reduced that of p38 and JNK. These results suggest that EGCG has a protective effect against regional myocardial I/R injuries through activation of the RISK pathway and attenuation of p38 and JNK. EGCG may have cardioprotective effects in patients undergoing surgeries prone to myocardial I/R injuries.