Neuroprotective effect of (-)-epigallocatechin-3-gallate in rats when administered pre- or post-traumatic brain injury
Neuroprotective effect of (-)-epigallocatechin-3-gallate in rats when administered pre- or post-traumatic brain injury
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DOI：
10.1007/s00702-012-0918-4
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发表时间：
2013-05-01
影响因子：
3.3
通讯作者：
Satou, Takao
中科院分区：
文献类型：
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作者：
Itoh, Tatsuki;Tabuchi, Masaki;Satou, Takao
我们先前的研究表明，在创伤性脑损伤(TBI)前后摄入(-)-表没食子儿茶素没食子酸酯(EGCG)可以消除大鼠自由基的产生，从而抑制神经元变性和细胞凋亡，改善认知功能障碍。在这里，我们研究了在颅脑损伤前后不同时间给予EGCG对脑功能和形态的影响。将Wistar大鼠分为5组，分别给予正常饮水、伤前EGCG、伤前和伤后EGCG、伤后EGCG和正常饮水假手术组。10周龄时用气动控制致伤装置致伤。免疫组织化学和脂质过氧化研究显示，伤后1、3、7d，EGCG各剂量组损伤区8-羟基-2‘-脱氧鸟苷、4-羟基-2-壬烯醛和单链DNA阳性细胞数及丙二醛水平均显著低于对照组(P<0.05)。尽管各EGCG治疗组脑损伤后存活神经元数量较水组显著增加(P<；0.05)，但认知功能障碍的改善仅在持续使用EGCG组和脑损伤后应用EGCG组有显著改善(P<；0.05)。这些结果表明，EGCG能抑制自由基诱导的脑损伤周围神经元的变性和细胞凋亡。重要的是，持续的和脑损伤后的EGCG治疗改善了脑损伤后的脑功能。综上所述，饮用绿茶可能是治疗脑外伤患者的一种有效方法。
Our previous study indicated that consuming (-)-epigallocatechin gallate (EGCG) before or after traumatic brain injury (TBI) eliminated free radical generation in rats, resulting in inhibition of neuronal degeneration and apoptotic death, and improvement of cognitive impairment. Here we investigated the effects of administering EGCG at various times pre- and post-TBI on cerebral function and morphology. Wistar rats were divided into five groups and were allowed access to (1) normal drinking water, (2) EGCG pre-TBI, (3) EGCG pre- and post-TBI, (4) EGCG post-TBI, and (5) sham-operated group with access to normal drinking water. TBI was induced with a pneumatic controlled injury device at 10 weeks of age. Immunohistochemistry and lipid peroxidation studies revealed that at 1, 3, and 7 days post-TBI, the number of 8-Hydroxy-2'-deoxyguanosine-, 4-Hydroxy-2-nonenal- and single-stranded DNA (ssDNA)-positive cells, and levels of malondialdehyde around the damaged area were significantly decreased in all EGCG treatment groups compared with the water group (P < 0.05). Although there was a significant increase in the number of surviving neurons after TBI in each EGCG treatment group compared with the water group (P < 0.05), significant improvement of cognitive impairment after TBI was only observed in the groups with continuous and post-TBI access to EGCG (P < 0.05). These results indicate that EGCG inhibits free radical-induced neuronal degeneration and apoptotic death around the area damaged by TBI. Importantly, continuous and post-TBI access to EGCG improved cerebral function following TBI. In summary, consumption of green tea may be an effective therapy for TBI patients.