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Kinetics of Apoptosis and Expression of Apoptosis-Related Proteins in Rat CA3 Hippocampus Cells After Experimental Diffuse Brain Injury

机译:实验性弥漫性脑损伤后大鼠CA3海马细胞凋亡动力学及相关蛋白的表达

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The present study examined kinetics of apoptosis and expression of apoptosis-related proteins Bcl-2, Bax, and caspase-3 in the CA3 hippocampus cells after diffuse brain injury (DBI) induced experimentally in rats. Percentage of apoptotic cells and expressions of above proteins were examined by flow cytometry and immunohistochemistry. Substantial neuronal apoptosis was documented in the CA3 hippocampus cells after DBI (22.26 ± 2.97 % at 72 h after DBI vs. 2.92 ± 0.88 % in sham-operated animals). Expression of Bc1-2 decreased, while expression of Bax and caspase-3 increased after DBI, with caspase-3 expression peaking after that of Bax (72 vs. 48 h, respectively). Further, the Bc1-2/Bax expression ratio decreased prior to increase of caspase-3 expression. In conclusion, cell apoptosis and altered expressions of Bcl-2, Bax, and caspase-3 are present in the CA3 region of hippocampus after experimental DBI. Changes in the Bc1-2/Bax expression ratio may facilitate activation of caspase-3 and aggravate neuronal apoptosis after brain injury.
机译:本研究检查了大鼠实验性弥漫性脑损伤(DBI)后海马CA3海马细胞凋亡的动力学以及凋亡相关蛋白Bcl-2,Bax和caspase-3的表达。通过流式细胞术和免疫组织化学检查凋亡细胞的百分比和上述蛋白的表达。在DBI后,CA3海马细胞中记录到大量神经元凋亡(DBI后72小时为22.26±2.97%,而假手术动物为2.92±0.88%)。 DBI后,Bc1-2的表达下降,而Bax和caspase-3的表达增加,而caspase-3的表达在Bax之后达到峰值(分别为72小时和48小时)。此外,在caspase-3表达增加之前,Bc1-2 / Bax表达比率降低。总之,实验性DBI后海马CA3区存在细胞凋亡和Bcl-2,Bax和caspase-3表达的改变。 Bc1-2 / Bax表达比的变化可能促进脑损伤后caspase-3的活化并加剧神经元凋亡。

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