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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（cPGES、mPGES－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；mPGES－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、cPGES、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。“,”Objective To investigate the change of PGs synthases-PGs-PGs receptor signal pathway in cerebral cortex of chronic a-luminum overload rat.Methods The chronic aluminum overload rats were induced via intragastric administration of aluminum gluconate ( Al3+200 mg/kg) , once a day, with 5d a week ,for total 20w.The functions of spatial learning and memory were evaluated by Morris wa-ter maze.Pathomorphological changes of rat cortical neurons were observed by HE staining.SOD activity and MDA content were detected by biochemistry methods.Changes of PGs levels in cortical tissues were assessed by ELISA, PGs synthase and PGs receptor mRNA expression were measured by RT-PCR, PGs receptor protein expression was measured by Western blot.Results Compared with those of control group, the spatial learning and memory functions were notably impaired in aluminum overload group, and the cortical neurons of aluminum overload rats appeared nuclear condensation.In the cerebral cortical tissues, the contents of PGE2, PGD2, PGF2α, 6-keto-PGF1α, TXB2 were in-creased.The mRNA expressions of mPGES-1, PGIS, TXAS, EP2, DP1, IP, EP4 were increased and EP3, FP, TP were decreased.The protein expressions of EP2, IP were increased and EP3 was decreased.Conclusions PGs synthase-PGs-PGs receptor signaling pathway dis-order is presented in cortical tissue of aluminum overload rat.However, further discussion on the specific mechanisms of the imbalance of signaling pathways induced by chronic aluminum overload in SD rat cerebral cortex is needed.