Role of G protein inhibitory α subunit 1/3 mediating the nerve growth factor pathway in postoperative learning and memory function in Alzheimer's disease mice
10.3969/j.issn.1009-0126.2025.11.026
- VernacularTitle:G蛋白抑制性α亚单位1和3介导神经生长因子通路在阿尔茨海默病小鼠术后学习记忆中的作用
- Author:
Cuicui SHI
1
;
Yufeng ZHANG
1
;
Hao ZHANG
1
;
Enhui CUI
1
;
Ming YAN
1
;
Yue SUN
1
;
Jian SUN
1
Author Information
1. 淮安市妇幼保健院麻醉科,江苏淮安 223002
- Publication Type:Journal Article
- Keywords:
Alzheimer's disease;
postoperative cognitive complications;
G protein inhibitory α subunit(Gαi)1/3;
nerve growth factor
- From:
Chinese Journal of Geriatric Heart Brain and Vessel Diseases
2025;27(11):1562-1566
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the effects of isoflurane anesthesia on cognitive function and the hippocampal nerve growth factor(NGF)and tyrosine receptor kinase A(TrkA)signaling pathway in Alzheimer's disease(AD)mice,while explore the role of G protein inhibitory α subunit 1/3(Gαi1/3)in this pathway.Methods Twelve wide-type mice and 48 APP/PS1(AD)mice(all males)were respectively assigned into a control group and 4 experimental groups,including AD,AD+postoperative cognitive dysfunction(POCD)group,empty adenovirus group,and Gαi1/3 overexpression group,with 12 mice in each group.Morris water maze and novel object recognition tests were conducted to assess the learning and memory function of each group;Western blotting was applied to detect the expression of amyloid P-protein 1-42(Aβ1-42),IL-6,TNF-α,synaptotagmin-1,synapsin-1,and NGF,p-TrkA,Gαi1/3,and p-Gab1 in hippocampal tissues.Results Compared with the control group and AD group,the avoidance incubation period in the AD+POCD group is significantly extended from days 2 to 4(P＜0.05),enhanced expression of Aβ1-42,IL-6,and TNF-α(P＜0.05),and reduced expression of synaptotagmin-1,synapsin-1,NGF,p-TrkA,Gαi1/3,and p-Gab1(P＜0.05).When compared with the AD+POCD group and the empty adenovirus group,the avoidance latency in the Gαi1/3 overexpression group was significantly shorted on days 2 to 4(P＜0.05),down-regulation of Aβ1-42(2.00±0.39 vs 3.38±0.38),IL-6(1.65±0.37 vs 3.36±0.39),and TNF-α(1.58±0.30 vs 2.90±0.31,P＜0.05),and up-regulation of synaptotagmin-1,synapsin-1,Gαi1/3,and p-Gab1(P＜0.05).Conclusion Isoflurane anesthesia can exacerbate POCD in AD mice,and overexpression of Gαi1/3 can improve cognitive function by activating the phosphorylation of Gab1.
