Objective This study aimed to investigate the protective effect and mechanism of melatonin(MT)in post-stroke cognitive impairment(PSCI).Methods Male C57BL/6J mice were randomly divided into Sham,Stroke,and Stroke+MT groups(n=7/group).Photothrombotic-induced stroke model mice were injected intraperitoneally with saline or MT(20 mg/kg)for 21 consecutive days after modeling.Behavioral tests were performed to examine the cognitive function of the mice,Nissl staining to detect neuronal damage,and Western blotting to detect apoptosis,synaptic plasticity and mitophagy.Results Compared with Sham mice,stroke mice showed a significantly reduction in the discrimination index in the novel object recognition test and the time spent in the novel arm of the Y maze.The number of neurons in the hippocampus and cortex were significantly reduced.The levels of proapoptotic proteins(Bax,cleaved Caspase-3)were upregulated,the levels of synapse-related proteins(PSD-95,Synaptophysin)were downregulated,and the levels of mitophagy-related proteins(PINK1,Parkin)were upregulated.MT sig-nificantly increased the discrimination index in the novel object recognition test and the time spent in the novel arm of the Y maze.The number of hippocampal and cortical neurons were significantly increased.The levels of proapoptotic proteins(Bax,cleaved Caspase-3)were downregulated,the levels of synapse-related proteins(PSD-95,Synaptophysin)were upregulated,and the levels of mitophagy-related proteins(PINK1,Parkin)were downregulated.Conclusion MT inhibited excessive mitophagy and ameliorated PSCI.
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