Epigallocatechin-3-gallate relieves thrombin-induced neuronal cell apoptosis after cerebral hemorrhage and related mechanisms

ObjectiveTo the neuro-protective effects of epigallocatechin-3-gallate (EGCG) on thrombin-induced damages on primary cortical neurons and related mechanisms. MethodsPrimary cortical neurons were cultivated in vitro for eight days and then divided into the following groups: a control group, a thrombin group, an EGCG group and an EGCG pre-treatment group. The neurons were exposed to 10 μmol/L EGCG for 24 h followed by treatment with 1×105 U/L thrombin for 24 h. Then, for the release of lactate dehydrogenase (LDH) was measured. Neuronal damage was assessed by flow cytometry. The levels of phosphorylated JNK and caspase-3 were determined by Western blotting. ResultsCompared with the control group, the thrombin group showed remarkable increases in the release of LDH and neural apoptosis, and the levels of activated p-JNK and capases-3 (P<0.01). Compared with the thrombin group, the thrombin pre-treatment group showed marked decreases in the release of LDH and neural apoptosis, and the levels of activated p-JNK and capases-3 (P<0.01). ConclusionEGCG can relieve thrombin-induced neuronal damage, which may be related with inhibition of the JNK signaling pathway.