| Objective: To investigate the protective effects of beraprost sodium onneurodegeneration induced by chronic aluminum overload in rats.Methods: The aluminum-overload models of SD rats were establishedby intragastric administration of aluminum gluconate (200mg Al3＋/kg)oncea day, and5d/w for20weeks. Two hours later, rats were intragastricallyadministered beraprost sodium (6,12, and24μg kg-1) after each aluminumadministration. The ability of spatial learning and memory function wasevaluated by Morris water maze. Morphologic changes of hippocampal andcortex neurons were observed by HE dyeing. Biochemistry detected theactivity of SOD and the content of MDA. The level of6-k-PGF1αin rat brainwas measured by ELISA. The expression of PGIS mRNA and IP mRNAwere detected by qRT-PCR, the IP protein was detected by WB.Results: The spatial learning and memory function of chronicaluminum overload rats were significantly impaired compared with thecontrol group. In model rats, hippocampal and cortex neuron showedmarkedly karyopycnosis. The SOD activity markedly decreased and theMDA content obviously increased. The level of6-k-PGF1αsignificantly increased. The mRNA expression of PGIS and IP in rat brain tissueobviously increased as well as IP protein.Compared with that of model group, the spatial learning and memoryfunction improved, the neurons were prevented from karyopycnosis andlosing in beraprost sodium groups. Beraprost sodium markedly decreasedthe activity of SOD and blunted the increase of MDA content. The level of6-k-PGF1αdecreased with significance. The expression of PGIS mRNA andIP mRNA decreased as well as IP protein in a dose-dependent manner in rathippocampus and cortex.Conclusions: PGIS-PGI2-IP signal pathway takes part inpathophysiological process of injured brain induced by chronic aluminumoverload in rats. Beraprost sodium, a prostacyclin receptor agonist, has anobviously neuroprotective effect on chronic aluminum overload-inducedinjury. |
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