Abdulloh Machin, Abdulloh and Imam Susilo, Imam and Djoko A Purwanto, Djoko Green tea and its active compound epigallocathechin-3-gallate (EGCG) inhibit neuronal apoptosis in a middle cerebral artery occlusion (MCAO) model. Journal of Basic and Clinical Physiology and Pharmacology, 32. pp. 319-325. ISSN ISSN:0792-6855E-ISSN:2191-0286

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Abstract

Abstract Objectives: To determine the effect of green tea with the active ingredient epigallocathechin-3-gallate (EGCG) on the inhibition of apoptosis in the middle cerebral artery occlusion (MCAO) model. Methods: Four month old male Rattus norvegicus rats with a body weight of 200-275 g was used for the MCAO model and divided into five groups, and the treatment was carried out for 7 days. Before being sacrificed, the subject had 1 cc of blood drawn for high mobility group box 1 (HMGB-1) examination using enzyme-linked immunosorbent assay (ELISA), and after being sacrificed, the brain tissue specimen was taken to examine caspase-3 and B-cell lymphoma 3 (BCL-3) using immunohistochemistry methods. Results: There was no significant difference in HMGB-1 results for the treatment group compared to the control group (P1: 384.20 ± 231.72 [p = 0.553]; P2: 379.11 ± 268.4 [p = 0.526]; P3: 284, 87 ± 276.19 [p = 0.140]; P4: 435.32 ± 279.95 [p = 0.912]). There is a significant increase in BCL-2 expression between the treatment group compared to the control group (P1: 2.58 ± 0.51 [p = 0.04]; P2: 3.36 ± 0.50 [p<0.001]; P3: 4.00 ± 0.42 [p<0.001]; P4: 3.60 ± 0.52 [p<0.001]). There was a significant difference in caspase-3 expression compared to the control group in the P3 group (P1: 4.33 ± 0.49 [p = 0.652]; P2: 4.09 ± 0.30 [p = 0.136]; P3: 3.58 ± 0.51 [p = 0.01]; P4: 3.89 ± 0.42 [p = 0.063]). There is no correlation between HMGB-1 and caspase-3 (r = -0.063; p = 0.613) or BCL-2 (r = -0.106; p = 0.396). There is significant negative correlation between caspase-3 and BCL-2 (r = -0.459; p = 0.000). Conclusions: Green tea with the active ingredient EGCG can inhibit neuronal cell death through the apoptotic pathway and not through the activation of HMGB-1.

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