Influences of CCK-8 on expressions of apoptosis-related genes in prefrontal cortex neurons of morphine-relapse rats
Influences of CCK-8 on expressions of apoptosis-related genes in prefrontal cortex neurons of morphine-relapse rats
复制标题
DOI：
10.1016/j.neulet.2016.08.028
复制
发表时间：
2016-09
影响因子：
2.5
通讯作者：
G. Ye;L. Tao;Chunling Ma;D. Wen;Lin-sheng Yu;Yanyan Fan;Haiyan Hu;Xi-ping Chen;Y. Chu;Yuan Gao;Cheng Gao;Hao-chen Wang
中科院分区：
文献类型：
--
作者：
G. Ye;L. Tao;Chunling Ma;D. Wen;Lin-sheng Yu;Yanyan Fan;Haiyan Hu;Xi-ping Chen;Y. Chu;Yuan Gao;Cheng Gao;Hao-chen Wang
为探讨CCK-8对吗啡复吸大鼠前额叶皮层神经元凋亡相关基因Bax、Bcl-2和Caspase-3表达的影响，采用条件性位置偏爱（CPP）技术，建立了CCK-8（0.01、0.1和1.0 μg，i.c.v）干预的有效、成功的吗啡复吸大鼠模型。将前额叶皮质制成切片，细胞浆进行化学染色。通过对神经元Bax、Bcl-2、Caspase-3的表达进行评分，并计算其各自对应的Bax/Bcl-2比值（Bax/Bcl-2）。结果表明：生理盐水组Bcl-2表达极弱，Bax和Caspase-3几乎不表达;吗啡组Bax和Caspase-3表达强，Bcl-2表达弱，与生理盐水组比较，差异有显著性（P< 0.05）; Bax、Caspase-3的表达及Bax/Bcl-2的比值在0.01 μg组、0.1 μg组、1.0 μg组依次呈逐渐降低趋势，而Bcl-2的表达则呈相反趋势，与吗啡组比较，除0.01 μg组外，差异均有显著性（P< 0.05）。结论：CCK-8（0.1和1.0 μg，i.c.v）可通过上调Bcl-2表达，下调Bax和Caspase-3表达，降低Bax/Bcl-2比值，对吗啡复吸大鼠前额叶皮层神经元起到保护作用。
In order to elucidate the influences of CCK-8 on expressions of apoptosis-related genes, Bax, Bcl-2 and Caspase-3, of prefrontal cortex neurons in morphine-relapse rats, an effective, successful morphine-relapse-rat model using the conditioned place preference (CPP) under CCK-8 (0.01, 0.1 and 1.0 μg, i.c.v) intervention was established. The prefrontal cortexes were made into slices with the cellular plasmas immunohistochemically stained. The expressions of Bax, Bcl-2, Caspase-3 of neurons were evaluated through their scores, and each corresponding ratio of Bax and Bcl-2 (Bax/Bcl-2) was also computed. The results showed that the expression of Bcl-2 was very weak and those of Bax and Caspase-3 were hardly seen in group normal saline; the expressions of Bax and Caspase-3 were strong and that of Bcl-2 was weak in group morphine and compared to group normal saline, there were significant differences (P< 0.05); the expressions of Bax, Caspase-3 and the ratios of Bax/Bcl-2 have a gradually-decreased trend in the sequence of group 0.01 μg, group 0.1 μg and group 1.0 μg, but the expression of Bcl-2 has an opposite trend in the same sequence, and compared to group morphine, there were significant differences (P< 0.05) excluding group 0.01 μg. So we draw a conclusion that CCK-8 (0.1 and 1.0 μg, i.c.v) could protect neurons of prefrontal cortex through up-regulating the expression of Bcl-2, down-regulating those of Bax and Caspase-3 and reducing Bax/Bcl-2 ratio in the model of morphine-relapse rats.