铝负荷致慢性脑损伤大鼠皮层前列腺素合酶-前列腺素-前列腺素受体信号通路变化特征

发布时间：2018-06-06 00:27

本文选题：铝负荷 + 大脑皮层　；参考：《中国老年学杂志》2015年07期

【摘要】：目的观察铝负荷致慢性脑损伤大鼠皮层前列腺素(PGs)合酶-PGs-PGs受体信号通路的变化特征。方法 SD雄性大鼠经灌胃给予葡萄糖酸铝溶液(Al3+200 mg/kg),1次/d,每周持续灌胃5 d,共20 w,建立慢性铝负荷致大鼠脑损伤模型。采用Morris水迷宫、组织病理学、生化酶学指标观察慢性铝负荷大鼠皮层神经元损伤,采用ELISA方法检测皮层组织PGs(PGD2、PGE2、PGF2α、6-keto-PGF1α、TXB2)含量变化,RT-PCR方法测定大鼠皮层PGs合酶(c PGES、m PGES-1、H-PGDS、PGIS、TXAS)和PGs受体(EP1、EP2、EP3、EP4、DP1、FP、TP、IP)mRNA表达,Western印迹方法检测皮层PGs受体(EP2、EP3、DP1、FP、TP、IP)蛋白含量。结果与对照组相比,慢性铝负荷大鼠空间学习记忆能力明显下降,皮层神经元核固缩;皮层组织SOD活性均降低,MDA含量增加;皮层PGE2、PGD2、PGF2α、6-keto-PGF1α、TXB2的含量均显著升高;m PGES-1、PGIS、TXAS、EP2、DP1、IP、EP4 mRNA表达明显升高,EP3、FP、TP mRNA表达明显降低,H-PGDS、c PGES、EP1 mRNA无明显变化;皮层EP2、IP蛋白表达显著升高,而EP3蛋白表达明显降低,DP1、FP、TP蛋白无明显变化。结论铝负荷大鼠的皮层PGs合酶-PGs-PGs受体信号通路平衡失调,其可能参与了铝负荷致大鼠皮层神经损伤机制。
[Abstract]:Objective to observe the changes of signal pathway of prostaglandin (PGs) synthase-PGs-PGs receptor in rats with chronic brain injury induced by aluminum load. Methods male SD rats were treated with aluminum gluconate solution (Al3 200 mg / kg) once a day for 5 days a week for 20 weeks to establish a brain injury model induced by chronic aluminum loading. Morris water maze, histopathological, biochemical and enzymatic indexes were used to observe the cortical neuron injury in rats with chronic aluminum loading. The ELISA method was used to detect the expression of PGF 2 伪 6-keto-PGF 1 伪 in cortical tissue. RT-PCR was used to detect the protein expression of PGs synthase c PGESm PGES-1H-PGISTXASand PGs receptor EP1EP2EP2EP4EP4EP4DP1DP1PP-PXB2.Western Western method was used to detect the protein content of PGs receptor EP2EP3DP1. Results compared with the control group, the spatial learning and memory ability of rats with chronic aluminum load was significantly decreased, the cortical neurons were pyknotic, the activity of SOD in cortex tissue was decreased and the content of SOD was increased. The content of TXB2 in PGE2P PGF2 伪 and PGF2 伪 PGF2 伪 was significantly increased, while the expression of PGES-1 PGES-1 PGES-1 IPEP4 mRNA was significantly increased, and the expression of PGE3 PGESEP1 mRNA was significantly decreased, while the expression of EP3 protein was not significantly decreased in PGE2IP, but the expression of EP3 was not significantly decreased in the cortex of PGE2PGF2 伪, but the expression of EP3 protein was not significantly decreased in PGE2P, PGESEP1, PGE2, PGE2, PGF2 伪, PGE2, PGF2, PGF2, PGF2, PGF2, PGF2, PGF2, PGF2, PGF2, PGF2, and PGE2. Conclusion the imbalance of PGs synthase-PGs-PGs receptor signaling pathway in aluminum-loaded rats may be involved in the mechanism of cortical nerve injury induced by aluminum load.
【作者单位】：重庆医科大学药理学教研室重庆市生物化学与分子药理学重点实验室;
【基金】：国家自然科学基金资助项目(No.81070972)
【分类号】：R966

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