<p>Cerebral protection of epigallocatechin gallate (EGCG) via preservation of mitochondrial function and ERK inhibition in a rat resuscitation model</p>

Abstract

Background Various and opposite roles of epigallocatechin gallate (EGCG) have been reported in different studies. We aimed to investigate how EGCG affects the cerebral injury in a cardiac arrest/cardiopulmonary resuscitation (CA/CPR) model of rat. Methods The rats which were subjected to CA/CPR randomly received low dose of EGCG (3 mg/kg, Low-EGCG group, n=16), high dose of EGCG (9 mg/kg, High-EGCG group, n=16) and equal volume of 0.9% saline solution (NS group, n=16) at the first minute after return of spontaneous circulation (ROSC). The rats underwent anesthesia and intubation were defined as Sham group (n=16). Twenty-four hours after ROSC, neural defect score (NDS), ROS fluorescence intensity, degree of mitochondrial permeability transition pore (mPTP) opening, ATP contents and mitochondrial ATP synthase expression were evaluated in the four groups. The expression of extracellular signal-regulated kinase (ERK) activity and cleaved-caspase 3 were also detected by Western blot. Results CA/CPR induced severe ischemia-reperfusion injury (IRI), resulted in mitochondrial dysfunction and upregulated phosphorylation of ERK. EGCG dose-dependently alleviated the IRI after CA/CPR, inhibited ERK activity and restored mitochondrial function and, as indicated by improved NDS, reduced ROS level, decreased mPTP opening, elevated ATP content, increased ATPase expression and downregulated cleaved-caspase 3 level. Conclusion EGCG alleviated global cerebral IRI by restoring mitochondrial dysfunction and ERK modulation in a rat CA/CPR model, which might make it a potential candidate agent against IRI after CA/CPR in the future. Further study is needed to determine whether higher dosage of EGCG might aggravate cerebral IRI post-CA/CPR.

Epigallocatechin-3-Gallate Suppresses the Expression of TNF-α-Induced MMP-1 <i>via</i> MAPK/ERK Signaling Pathways in Human Dermal Fibroblasts

“…Existing studies report IC 50 of 13 µM for DPPH elimination with EGCG, suggesting that the results of the current study are similar to previous results. 18) It was found that EGCG suppressed ROS production in fibroblasts treated with TNF-α. EGCG has been reported to suppress ROS production in damaged brain tissues.…”

Novel controlled and targeted releasing hydrogen sulfide system exerts combinational cerebral and myocardial protection after cardiac arrest

“…Sprague-Dawley rats were anesthetized and heparinized (0.2 mL, I.P.). Then the CA/CPR rat model was established by the previous method [30] (described in Additional file 1). Rats were randomized into three groups: (1) sham (n = 6), which were subjected to the same procedure as the other groups except for CA/CPR; (2) Control group (n = 6), which underwent 5 min of CA and received injection of same volume of saline; (3) DATS@MION-PEG-LF group (n = 6), which underwent 5 min of CA and received injection of DATS@MION-PEG-LF (10 mg/kg).…”

Epigallocatechin-3-gallate protects cardiomyocytes from hypoxia-reoxygenation damage via raising autophagy related 4C expression

“…Qin et al . [ 43 ], discovered that EGCG played cerebral protective activity after I/R injury via elevating ATP level. In this study, we found that EGCG raised the ATP level in H/R-treated H9c2 cells.…”