Green tea and its active compound epigallocathechin-3-gallate (EGCG) inhibit neuronal apoptosis in a middle cerebral artery occlusion (MCAO) model

医学 细胞凋亡 免疫组织化学 大脑中动脉 闭塞 没食子酸 绿茶 传统医学 胃肠病学 半胱氨酸蛋白酶3 内科学 内分泌学 药理学 化学 生物化学 缺血 程序性细胞死亡 食品科学
作者
Abdulloh Machin,Imam Susilo,Djoko Agus Purwanto
出处
期刊:Journal of basic and clinical physiology and pharmacology [De Gruyter]
卷期号:32 (4): 319-325 被引量:11
标识
DOI:10.1515/jbcpp-2020-0454
摘要

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.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.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).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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