Objective Our objective was to examine the potential of cerebroprotein hydrolysate for injection I(CH-I)in mitigating oxidative stress,apoptosis,and neuroinflammation in an Alzheimer's disease(AD)model,while also gaining a better understanding of the underlying mechanisms.Methods AD mouse model was established through the intrahippocampal injection of amyloid-β142.The experiment consisted of four groups:Control(Con)group,Aβ group,Aβ+CH-I group,and CH-I group.The learning and memory abilities of the mice were assessed using the new object recognition experiment and Y-maze.Enzyme-linked immunosorbent assay was employed to measure the activity of superoxide dismutase(SOD),glutathione peroxidase(GSH-Px),thioredoxin,and catalase(CAT)in brain tissue.Additionally,Tunel staining was utilized to evaluate the levels of cell apoptosis.Aβ group and Aβ+CH-I group were extracted for RNA-seq and bioinformatics analysis and verification.Western blotting analysis was conducted to detect proteins associated with the pathway[c-Jun N-terminal kinase(JNK),mitogen-activated protein kinase(MAPK),p38 MAPK].Results In comparison to the Con group and the Aβ+CH-I group,the Aβgroup exhibited a significant decrease in the proportion of time allocated to exploring novel arms/objects.Moreover,the Aβ group displayed significantly lower levels of SOD and GSH-Px activities in mice,in contrast to both the Con group and the Aβ+CH-I group,with statistically significant distinctions.The RNA-seq analysis demonstrated a significant downregulation of the MAPK signaling pathway in the Aβ+CH-I group compared to the Aβ group.Additionally,the Aβ+CH-I group exhibited noteworthy reductions in apoptosis levels,p38 MAPK protein,and inflammation levels when compared to the Aβ group.Conclusions CH-I exerts neuroprotective effects through the modulation of the p38 MAPK signaling pathway,thereby conferring neuronal resistance against oxidative stress and apoptosis.
维普
万方数据
