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김석재,Mei Li,정철원,배홍범,학상현,이승현,이현정,Bong Ha Heo,육근배,유경연 대한약학회 2014 Archives of Pharmacal Research Vol.37 No.8
Epigallocatechin-3-gallate (EGCG), the majorcatechin derived from green tea, has been shown to modulatenumerous molecular targets in the setting of inflammation. This study aimed to determine whether EGCGprotects against regional myocardial ischemia/reperfusion(I/R) injuries and its underlying mechanisms involving therole of reperfusion injury salvage kinase (RISK) pathways(PI3K-Akt and ERK 1/2) and GSK-3b or apoptotic kinases(p38 and JNK). The rats were subjected to I/R injuriesconsisting of 30 min ischemia followed by 2 h reperfusion. EGCG (10 mg/kg, intravenously) was administered aloneor 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-3b, and MAPKkinases (ERK1/2, P38 and JNK) was determined by Westernblotting after 10 min of reperfusion. EGCG reducedthe infarct size compared with the control (25.4 ± 9.2versus 43.2 ± 8.2 %, p\0.05). Wortmannin alone did notaffect the infarct size, but abolished the EGCG-induced infarct size limiting effect, indicating that EGCG mayprotect the heart by modulating the PI3K-Akt. EGCGsignificantly enhanced the phosphorylation of Akt andGSK-3b but not ERK1/2, while it reduced that of p38 andJNK. These results suggest that EGCG has a protectiveeffect against regional myocardial I/R injuries throughactivation of the RISK pathway and attenuation of p38 andJNK. EGCG may have cardioprotective effects in patientsundergoing surgeries prone to myocardial I/R injuries.
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