| [Background] Neuronal injury is a pathological phenomenon in nervous system diseases such as neurodegenerative disease,brain injury,cerebral ischemia and so on,and affects the occurrence and development of the disease.It can prevent and treat neurological diseases by improving the damage of brain neurons and restoring their normal cell function.It was found that the endogenous ligand of G protein-coupled receptor APJ,Apelin-13,can improve the neuron damage caused by the disease state,thus achieving the purpose of treating the disease.However,the specific mechanism by which Apelin-13 can improve the neuron damage is still unclear.Studies have reported that one of the important roles of BDNF is directly involved in the improvement of hippocampal neuron damage.Subunit of peroxisome proliferator-activated receptor-γ coactivator-1 alpha,proliferator-activated receptor-γ proliferator PGC-1α)and fibronectin type Ⅲ domain-containing protein 5(FNDC5)play an important role in energy metabolism.Studies have shown that there is an interaction between PGC-1α/FNDC5/BDNF,and the expression of PGC-1α/FNDC5/BDNF is decreased in disease state,suggesting that the regulation of their expression may be a potential target for the treatment of nervous system diseases.Meanwhile,studies have shown that Apelin-13 can regulate the expression of BDNF in the hippocampus and have a protective effect on the nervous system.Therefore,in this study,mouse hippocampal neuronal HT22 cells were taken as the object of study to investigate whether Apelin-13 could regulate the expression of PGC-1α/FNDC5/BDNF and thus have a neuroprotective effect on mouse hippocampal neuronal HT22 cells.[Method] PGC-1α/FNDC5 of mouse hippocampal neuron HT22 cells were induced by low expression of si RNA,and then Apelin-13 was treated on the basis of low expression induced injury.Protein expression was detected by Western Blot,m RNA level was detected by RT-q PCR,cell death was detected by Hoechst/PI staining,and cell apoptosis was detected by flow cytometry.To observe whether Apelin-13 could affect the expression of PGC-1α/FNDC5/BDNF,and then improve the hippocampal neuronal HT22 cell injury induced by low expression of PGC-1α/FNDC5.[Results] The low expression of si RNA in mouse hippocampal neuron HT22 cell PGC-1α/FNDC5 resulted in significantly up-regulated HT22 cell death rate and apoptosis rate,resulting in significant cell damage,and down-regulated PGC-1α/FNDC5/BDNF expression.Apelin-13 promoted the expression of PGC-1α/FNDC5/BDNF in mouse hippocampal neuron HT22 cells.Apelin-13 can improve the cell damage caused by PGC-1α/FNDC5 in the hippocampal neurons of mice with low si RNA expression,and meanwhile up-regulate the expression of PGC-1α,FNDC5 and BDNF in the hippocampal neurons of mice with low si RNA expression.[Conclusion] Apelin-13 may have a protective effect on mouse hippocampal neuron HT22 cells through PGC-1α/FNDC5/BDNF pathway. |