Effect of SS31 peptide on cognitive function and oxidative stress in cerebral cortex of Alzheimer's disease model mice
10.3760/cma.j.cn371468-20250101-00002
- VernacularTitle:SS31肽对阿尔茨海默病模型小鼠认知功能及大脑皮质氧化应激的影响
- Author:
Yiming YANG
1
;
Yanli JIA
;
Jianhua WANG
;
Kun LI
Author Information
1. 河北北方学院附属第一医院病理科,张家口 075000
- Publication Type:Journal Article
- Keywords:
Alzheimer's disease;
SS31 peptide;
Cognitive function;
Cerebral cortex;
Oxidative stress;
Neuronal apoptosis;
APP/PS1 mouse
- From:
Chinese Journal of Behavioral Medicine and Brain Science
2025;34(6):488-494
- CountryChina
- Language:Chinese
-
Abstract:
Objective:To investigate the effects of SS31 peptide on cognitive function and cortical oxidative stress in Alzheimer's disease (AD) model mice.Methods:Eighteen SPF grade male 8-month-old APP/PS1 mice were randomly divided into model group and SS31 group according to the random number table method, with nine mice in each group. Additionally, nine C57BL/6J mice with matched weight were selected as the control group. The mice in SS31 group were intraperitoneally injected with SS31 peptide (3 mg/kg, 0.3 mg/mL), while the mice in model group and control group were intraperitoneally injected with an equal volume of 0.9% NaCl solution.The response ability and daily living ability of mice were evaluated by nest building test (NBT).The learning, memory and exploration abilities of mice were assessed by new object recognition (NOR) and Morris water maze test (MWM). ELISA was used to detect the levels of β -amyloid protein (Aβ) and reactive oxygen species (ROS) in cerebral cortex of mice, and immunofluorescence (IF) was used to detect the number of Aβ plaques.Flow cytometry was used to detect neuronal apoptosis rate, Nissl staining was used to detect neuronal damage, and transmission electron microscopy was used to observe neuronal and mitochondrial morphology. Statistical analysis was conducted by SPSS 25.0 software. One-way ANOVA or repeated measures ANOVA or Kruskal-Wallis H test were used for multi-group comparison. Results:(1) The cognitive evaluation results showed that there were statistically significant differences in NBT latency, 15 hour nest building score, and NOR recognition index among the 3 groups of mice ( F=5.488, 6.750, 10.379, all P<0.05), as well as the platform crossing frequency( H=6.742, P<0.05).The time and group interaction of MWM escape latency in the 3 groups of mice were not significant( F=0.975, P=0.460), but the main effect of time and group were significant( F=14.011, 4.173, both P<0.05).The percentage of platform quadrant dwell time in the model group ((22.91 ± 5.16)%) was lower than that in the control group ((39.96±4.69)%) ( P<0.05), but there was no statistically significant difference compared to the SS31 group ((25.18±3.04)%) ( P>0.05). (2) The ELISA results showed that there were statistically significant differences in the levels of Aβ40, Aβ42 and ROS in cerebral cortex of the 3 groups of mice ( F=12.634, 43.670, 7.143, all P<0.01).All the above indicators of cerebral cortex in the model group were higher than those in control group and SS31 group (all P<0.05). The IF results also confirmed that the numbers of Aβ40 and Aβ42 plaques in cerebral cortex of the model group were higher than those of the control group and SS31 group (all P<0.05). (3) The results of flow cytometry and Nissl staining showed that there were statistically significant differences in the apoptosis rate and injury rate of cortical neurons among the 3 groups of mice ( F=234.086, 43.800, both P<0.05), and the two indicators of cortical neurons in the model group were higher than those in control group and SS31 group (all P<0.05). The transmission electron microscopy results showed that compared with the control group, the structure and morphology of cortical neurons and mitochondria in the model group were abnormal, while the structure and morphology of the SS31 group were close to normal. Conclusion:SS31 peptide can improve cognitive function in AD model mice by inhibiting oxidative stress and neuronal apoptosis in cerebral cortex.