scholarly journals Electroacupuncture Improves Cognitive Function in Senescence-Accelerated P8 (SAMP8) Mice via the NLRP3/Caspase-1 Pathway

2020 ◽  
Vol 2020 ◽  
pp. 1-14
Author(s):  
Zhitao Hou ◽  
Ruijin Qiu ◽  
Qingshuang Wei ◽  
Yitian Liu ◽  
Meng Wang ◽  
...  
Keyword(s):  
Cognitive Function ◽  
Signaling Pathway ◽  
Tau Proteins ◽  
Morris Water Maze Test ◽  
Control Group ◽  
Caspase 1 ◽  
Cell Counts ◽  
Tnf Α ◽  
Hippocampal Morphology ◽  
Samp8 Mice

Background. Clinically, electroacupuncture (EA) is the most common therapy for aging-related cognitive impairment (CI). However, the underlying pathomechanism remains unidentified. The aims of this study were to observe the effect of EA on cognitive function and explore the potential mechanism by which EA acts on the NLRP3/caspase-1 signaling pathway. Main Methods. Thirty male SAMP8 mice were randomly divided into the model, the 2 Hz EA and 10 Hz EA groups. Ten male SAMR1 mice were assigned to the control group. Cognitive function was assessed through the Morris water maze test. Hippocampal morphology and cell death were observed by HE and TUNEL staining, respectively. The serum IL-1β, IL-6, IL-18, and TNF-α levels were measured by ELISA. Hippocampal NLRP3, ASC, caspase-1, GSDM-D, IL-1β, IL-18, Aβ, and tau proteins were detected by Western blotting. Key Findings. Cognitive function, hippocampal morphology, and TUNEL-positive cell counts were improved by both EA frequencies. The serum IL-1β, IL-6, IL-18, and TNF-α levels were decreased by EA treatment. However, 10 Hz EA reduced the number of TUNEL-positive cells in the CA1 region and serum IL-1β and IL-6 levels more effectively than 2 Hz EA. NLRP3/caspase-1 pathway-related proteins were significantly downregulated by EA, but 2 Hz EA did not effectively reduce ASC protein expression. Interestingly, both EA frequencies failed to reduce the expression of Aβ and tau proteins. Significance. The effects of 10 Hz EA at the GV20 and ST36 acupoints on the NLRP3/caspase-1 signaling pathway may be a mechanism by which this treatment relieves aging-related CI in mice.

scholarly journals Preoperative pain aggravates postoperative cognitive deficits and hippocampal neuroinflammation in rats

2019 ◽  
Author(s):  
Xiang Gao ◽  
Xian Ding ◽  
Huan Yi ◽  
Chuan-tao Lin ◽  
Yu-ping Wang ◽  
...  
Keyword(s):  
Cognitive Function ◽  
Inflammatory Factors ◽  
Control Group ◽  
Gamma Aminobutyric Acid ◽  
Sprague Dawley ◽  
Preoperative Pain ◽  
Pain Model ◽  
Simple Operation ◽  
Tnf Α ◽  
Operation Group

Abstract Background Perioperative neurocognitive disorder (PND) is the progressive deterioration of cognitive function after surgery. The purpose of this study was to observe the effect of preoperative pain on inflammatory factors and neuronal apoptosis in the hippocampus of rats. Methods 36 adult male Sprague-Dawley rats were randomly divided into 4 groups: the control group, the pain group, the pain+operation group, and the operation group. 6 days before the surgery, the rats received cognitive training, and the cognitive evaluation was carried out on the1, 3 and 7th days after the surgery. The rats were killed on the first, third and seventh days after the surgery (n = 3 rats/day). The cognitive function of rats was evaluated by the Morris Water Maze (MWM), and the expression levels of the pro-inflammatory cytokines interleukin 6(IL-6), Interleukin 1β(IL-1β)and Tumor Necrosis Factor-α(TNF-α), Acetylcholine(Ach)and Cyclic Adenosine monophosphate(cAMP), protein kinase A(PKA)and gamma-aminobutyric acid type A receptors(GABAA) in the hippocampus were measured on the 1st, 3rd and 7th days after the operation. Results Our results showed that the pain model rats exhibited impaired behavior on the first day (P< 0.001), and this lasted until the 7th day after the operation (P≤0.002 and P≤0. 001, respectively). Preoperative pain model rats showed a higher level of apoptosis than that shown by the simple operation rats. On the 1st, 3rd and 7th days after the operation, the protein content of IL-1β, IL-6 and TNF-α in the pain operation group was increased compared to that in the simple operation group (P<0.001). ACh, cAMP, PKA and GABAA expression in the hippocampus was decreased after operation in the preoperative pain model rats. Conclusion Preoperative pain is a key risk factor for the development of PND. The ACh-PKA-GABAA signaling pathway plays a key role in the acetylcholine pathway.

scholarly journals Comparative Transcriptome Analysis Reveals the Protective Mechanism of Glycyrrhinic Acid for Deoxynivalenol-Induced Inflammation and Apoptosis in IPEC-J2 Cells

2020 ◽  
Vol 2020 ◽  
pp. 1-17
Author(s):  
Xiaoxiang Xu ◽  
Guorong Yan ◽  
Juan Chang ◽  
Ping Wang ◽  
Qingqiang Yin ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Signaling Pathway ◽  
Transcriptome Analysis ◽  
Animal Feed ◽  
Control Group ◽  
Protective Mechanism ◽  
Dependent Manner ◽  
Gene Expressions ◽  
Lactate Dehydrogenase Release ◽  
Tnf Α

Deoxynivalenol (DON) is the most common mycotoxin that frequently contaminates human food and animal feed, resulting in intestinal diseases and systemic immunosuppression. Glycyrrhinic acid (GA) exhibits various pharmacological activities. To investigate the protective mechanism of GA for DON-induced inflammation and apoptosis in IPEC-J2 cells, RNA-seq analysis was used in the current study. The IPEC-J2 cells were treated with the control group (CON), 0.5 μg/mL DON, 400 μg/mL GA, and 400 μg/mL GA+0.5 μg/mL DON (GAD) for 6 h. Results showed that 0.5 μg/mL DON exposure for 6 h could induce oxidative stress, inflammation, and apoptosis in IPEC-J2 cells. GA addition could specifically promote the proliferation of DON-induced IPEC-J2 cells in a dose- and time-dependent manner. In addition, GA addition significantly increased Bcl-2 gene expression ( P < 0.05 ) and superoxide dismutase and catalase activities ( P < 0.01 ) and decreased lactate dehydrogenase release, the contents of malonaldehyde, IL-8, and NF-κB ( P < 0.05 ), the relative mRNA abundances of IL-6, IL-8, TNF-α, COX-2, NF-κB, Bax, and caspase 3 ( P < 0.01 ), and the protein expressions of Bax and TNF-α. Moreover, a total of 1576, 289, 1398, and 154 differentially expressed genes were identified in CON vs. DON, CON vs. GA, CON vs. GAD, and DON vs. GAD, respectively. Transcriptome analysis revealed that MAPK, TNF, and NF-κB signaling pathways and some chemokines played significant roles in the regulation of inflammation and apoptosis induced by DON. GA may alleviate DON cytotoxicity via the TNF signaling pathway by downregulating IL-15, CCL5, and other gene expressions. These results indicated that GA could alleviate DON-induced oxidative stress, inflammation, and apoptosis via the TNF signaling pathway in IPEC-J2 cells.

Acupuncture promotes expression of Hsp84/86 and delays brain ageing in SAMP8 mice

2019 ◽  
Vol 37 (6) ◽  
pp. 340-347 ◽  
Author(s):  
Shichen Chang ◽  
Xuanyang Guo ◽  
Guomin Li ◽  
Xuezhu Zhang ◽  
Jing Li ◽  
...  
Keyword(s):  
Cognitive Function ◽  
Protein Expression ◽  
Success Rate ◽  
Superoxide Anion ◽  
Acupuncture Treatment ◽  
Protein Carbonyl ◽  
Morris Water Maze Test ◽  
Brain Ageing ◽  
Mrna And Protein Expression ◽  
Samp8 Mice

Objective: To study the effects of acupuncture on expression of heat shock protein (Hsp) 84 and 86, and brain ageing, in the senescence accelerated mouse prone 8 (SAMP8) model of Alzheimer’s disease. Methods: 7-month-old male senescence resistant mouse strain 1 (SAMR1) and SAMP8 mice were assigned to the following groups, with 15 animals in each group: SAMR1 control (Rc), SAMP8 control (Pc), SAMP8 acupuncture (Pa), SAMP8 sham-acupuncture (Psa). The Pa group was given acupuncture treatment once daily for 15 days. Neuromuscular coordination and cognitive function of the mice were evaluated by the tightrope test and Morris water maze test, respectively. The number of neurons in the CA1, CA3 and dentate gyrus (DG) regions of the hippocampus were measured. The levels of oxidative stress and protein carbonyl, mRNA and protein expression levels of Hsp84 and Hsp86 in the hippocampus were detected. Results: Compared with the Rc group, in the Pc mice there was a lower success rate for the tightrope test, impaired cognitive abilities, a decline in neuron numbers, reduced levels of superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px), increased levels of superoxide anion and protein carbonyl, and decreased mRNA and protein levels of Hsp84 and Hsp86 (all P<0.05). After acupuncture treatment, the success rate for the tightrope test was elevated, cognitive function was improved, neuron numbers were enhanced, levels of SOD and GSH-Px were increased, levels of superoxide anion and protein carbonyl were decreased, and Hsp84 and Hsp86 mRNA and protein expression were increased in the Pa mice when compared with the Pc and Psa groups (all P<0.05). Conclusion: Acupuncture may delay brain ageing in SAMP8 mice by reducing oxidative protein damage and promoting Hsp84 and Hsp86 expression.

scholarly journals Manual Acupuncture Suppresses the Expression of Proinflammatory Proteins Associated with the NLRP3 Inflammasome in the Hippocampus of SAMP8 Mice

2017 ◽  
Vol 2017 ◽  
pp. 1-8 ◽  
Author(s):  
Ning Ding ◽  
Jing Jiang ◽  
Menghan Lu ◽  
Jiatong Hu ◽  
Yiyuan Xu ◽  
...  
Keyword(s):  
Learning And Memory ◽  
Spatial Learning ◽  
Nlrp3 Inflammasome ◽  
Control Group ◽  
Spatial Learning And Memory ◽  
Manual Acupuncture ◽  
Caspase 1 ◽  
Donepezil Hydrochloride ◽  
Related Proteins ◽  
Samp8 Mice

Objective. To investigate the effect of manual acupuncture (MA) on NLRP3 inflammasome-related proteins. Methods. SAMP8 mice were randomly divided into Alzheimer’s disease (AD) group, the MA group, and the medicine (M) group. Mice in the M group were treated with donepezil hydrochloride at 0.65 μg/g. In the MA group, MA was applied on Baihui (GV20) and Yintang (GV29) for 20 min and then pricked at Shuigou (GV26). The Morris water maze was applied to assess spatial learning and memory. Immunohistochemical staining and western blot analysis were used to observe the expression of NLRP3 inflammasome-related proteins. Results. Compared with the normal (N) control group, spatial learning and the memory capabilities of the AD group significantly decreased (p<0.01). The number of NLRP3, ASC, Caspase-1, and IL-1β positively stained cells in the AD group was higher than the N group, and the relative expression levels of the above proteins were significantly higher than those in the N group (p<0.01). These changes were reversed by both MA and donepezil (p<0.01). Conclusion. MA can improve the learning and memory capabilities of SAMP8 mice. The negative regulation of the NLRP3/Caspase-1 pathway in the hippocampus may be a possible mechanism of MA in the treatment of AD.

scholarly journals Protective effects of ginkgolide on a cellular model of Alzheimer’s disease via suppression of the NF-κB signaling pathway

2021 ◽  
Author(s):  
Tiantong Niu ◽  
He Yin ◽  
Baolei Xu ◽  
Tingting Yang ◽  
Huiqin Li ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Cell Viability ◽  
Mrna Expression ◽  
Signaling Pathway ◽  
Hek293 Cells ◽  
Control Group ◽  
Cellular Model ◽  
Intracellular Protein ◽  
Tnf Α

Abstract NF-κB signaling has been reported to play a key regulatory role in the pathogenesis of Alzheimer’s disease (AD). The purpose of this study is to investigate the effects of ginkgolide on cell viability in an AD cellular model involving an APP/PS1 double gene-transfected HEK293 cell line (APP/PS1-HEK293) and further explored the mechanisms of action related to NF-κB signaling. The optimal time point and concentration of ginkgolide for cell proliferation were screened using a cell counting kit-8 assay. Based on the results, an in vitro study was performed by co-culture of APP/PS1-HEK293 with different dosages of ginkgolide, followed by an enzyme-linked immunosorbent assay to measure the levels of supernatant tumor necrosis factor (TNF)-α, interleukin (IL)-1β and IL-6, as well as western blotting and real-time polymerase chain reaction to detect intracellular protein and mRNA expression of NF-κB p65, IκBa, Bcl-2 and Bax. APP/PS1-HEK293 cells exhibited the highest cell viability at a concentration of 100 µg/ml after 48 h of treatment with ginkgolide. The supernatant levels of TNF-α, IL-1β and IL-6 in the high-dosage ginkgolide-treated groups were lower than those in the control group. Compared with the control group, there were decreased intracellular protein and mRNA expression of NF-κB p65 and Bax, but increased protein and mRNA expression of IκBa in both high-dosage and low-dosage group. Ginkgolide may enhance cell viability, indicative of its neuroprotective effects on AD, at least partially via suppression of the NF-κB signaling pathway involving anti-apoptosis and anti-inflammation mechanisms. Therefore, ginkgolide might be a promising therapeutic agent against AD.

scholarly journals Octreotide ameliorates hypoxia/reoxygenation-induced cerebral infarction by inhibiting oxidative stress, inflammation and apoptosis, and via inhibition of TLR4/MyD88/NF-κB signaling pathway

2021 ◽  
Vol 20 (11) ◽  
pp. 2261-2266
Author(s):  
Yanbin Hou ◽  
Zhongze Lou ◽  
Yunxin Ji ◽  
Liemin Ruan ◽  
He Gao
Keyword(s):  
Oxidative Stress ◽  
Cerebral Infarction ◽  
Signaling Pathway ◽  
Control Group ◽  
N2a Cells ◽  
Tnf Α ◽  
Octreotide Treatment ◽  
Vitro Model ◽  
Hypoxia Reoxygenation

Purpose: To explore the effects of octreotide (OCT) on oxidative stress, inflammation and apoptosis in hypoxia/reoxygenation (H/R)-induced cerebral infarction.Methods: The in vitro model of cerebral infarction was established by treating N2A cells with hypoxia for 4 h and reoxygenation for 24 h. The viability of N2A cells was determined by CCK-8 assay. The cells were divided into 3 groups: control group, H/R group, and H/R+OCT group. The cells in H/R+OCT group were pretreated with OCT (60 ng/mL) before H/R treatment. The oxidative stress of N2A cells were assessed by determining the levels of superoxide dismutase (SOD), glutathione peroxidase (GSHPx), catalase (CAT), reactive oxygen species (ROS) and malondialdehyde (MDA). Inflammation of N2A cells was evaluated by evaluating the levels of TNF-α, IL-1β, IL-6, and IL-8, while the apoptosis of N2A cells was assessed by flow cytometry. Western blot analysis was used to determine the expression of Bcl-2, Bax, TLR4, MyD88, and NF-κB.Results: Octreotide treatment significantly reduced the level of oxidative stress. The inflammation of N2A cells caused by hypoxia/reoxygenation was inhibited by treatment with octreotide. Apoptosis of N2A cells was also inhibited by octreotide treatment. Hypoxia/reoxygenation activated TLR4/MyD88/NF-κB signaling pathway, while octreotide inhibits the activation of this pathway.Conclusion: The results reveal that octreotide inhibits hypoxia/reoxygenation-induced oxidative stress,as well as the inflammation, and apoptosis of N2A cells by inhibiting TLR4/MyD88/NF-κB signaling pathway. Thus, these findings may provide new insights into the treatment of cerebral infarction.

scholarly journals Sevoflurane and fentanyl exert protective effect on cognitive function in aged rats via regulation of inflammatory response in the brain

2021 ◽  
Vol 18 (5) ◽  
pp. 961-965
Author(s):  
Xin Zhao ◽  
Peixiang Li
Keyword(s):  
Cognitive Function ◽  
Inflammatory Response ◽  
Control Group ◽  
Vascular Endothelial ◽  
Aged Rats ◽  
Tnf Α ◽  
Male Wistar Rats ◽  
Factor Α ◽  
Endothelial Growth Factor ◽  
The Brain

Purpose: To investigate the effects of sevoflurane and fentanyl on cognitive function in aged rats, and to determine the mechanism of action. Methods: A total of 160 adult male Wistar rats were randomly assigned to four groups of 40 rats each. With the exception of control, the rats were surgically operated on. Sevoflurane group received sevoflurane (2 %) via inhalation for 2 h/day for 7 days, while the fentanyl group received fentanyl (50 µg/kg body weight) for 1 h via their tail veins for 7 days. The cognitive function of the rats was evaluated by shuttle box and Morris water maze (MWM) tests, while interleukin-6 (IL-6), vascular endothelial growth factor (VEGF) and tumor necrosis factor α (TNF-α) were evaluated using ELISA kits. Results: The learning and memory latencies of the rats were significantly prolonged in surgery, with prolongation greater in sevoflurane and fentanyl groups than in control group; however, the latencies were significantly shorter in sevoflurane and fentanyl groups than in surgery group (p < 0.05). The levels of VEGF, IL-6 and TNF-α were significantly higher in the surgery, sevoflurane and fentanyl groups than in control group (p < 0.05). Conclusion: Sevoflurane and fentanyl improve cognitive function in aged rats via a mechanism involving the regulation of inflammatory response in the brain.

scholarly journals Berberine Reduces Renal Cell Pyroptosis in Golden Hamsters with Diabetic Nephropathy through the Nrf2-NLRP3-Caspase-1-GSDMD Pathway

2021 ◽  
Vol 2021 ◽  
pp. 1-13
Author(s):  
Baozhu Ding ◽  
Songyan Geng ◽  
Xiaojie Hou ◽  
Xuelian Ma ◽  
Huazhou Xu ◽  
...  
Keyword(s):  
Blood Glucose ◽  
Blood Lipids ◽  
Kidney Tissue ◽  
Inflammatory Factors ◽  
Control Group ◽  
Model Group ◽  
Golden Hamsters ◽  
Caspase 1 ◽  
Tnf Α ◽  
Nrf2 Expression

Objective. To observe the effect of berberine (BBR) on kidney cell pyroptosis in golden hamsters with diabetic nephropathy (DN) and to explore the molecular mechanism of its renal protection. Methods. Fifty clean-grade male golden hamsters were randomly divided into a control group (10) and a model building group (40). The DN model was established by high-sugar and high-fat feeding and injection of a small amount of STZ. After successful establishment of the model, they were randomly divided into a model group, western medicine group, and berberine high- and low-dose groups. The western medicine group was given irbesartan 13.5 mg/kg, and the berberine high- and low-dose groups were given BBR 200 mg/kg and 100 mg/kg, respectively, for 8 consecutive weeks. An automatic biochemical analyser was used to measure blood glucose, blood lipids, kidney function, MDA, and other indicators; radioimmunoassay was used to assess serum insulin; enzyme-linked immunosorbent assay (ELISA) was used to quantify IL-1β, IL-6, IL-18, TNF-α; HE, PAS, and Masson staining were used to observe kidney pathological tissue morphology; western blot and real-time fluorescent quantitative PCR were used to assess protein and mRNA expression of molecules, such as Nrf2, NLRP3, Caspase-1, and GSDMD; and TUNEL staining was used to detect DNA damage. SPSS statistical software was used for the data analysis. Results. The kidney tissues of golden hamsters in the control group were normal; Nrf2 was highly expressed, serum MDA level was low, NLRP3 expression in kidney tissue was not obvious, Caspase-1 and GSDMD were weakly expressed, and only a few TUNEL-positive cells were observed. Compared with the control group, the golden hamsters in the model group had obvious renal pathological damage; blood glucose, blood lipids, renal function-related indexes, insulin, and inflammatory factors IL-1β, IL-6, IL-18, and TNF-α were increased ( P < 0.05 ); NLRP3, Caspase-1, and GSDMD expression was increased; Nrf2 expression was decreased; MDA level was increased ( P < 0.05 ); and the number of TUNEL-positive cells was increased. Compared with the model group, the pathological morphology of the kidney tissue of golden hamsters in the three treatment groups was significantly improved; blood glucose, blood lipids, renal function, and the expression of inflammatory factors IL-1β and IL-6 were reduced ( P < 0.05 ); NLRP3, Caspase-1, GSDMD, and other molecular proteins and mRNA expression were decreased; Nrf2 expression was increased; MDA level was decreased ( P < 0.05 ); and the number of TUNEL-positive cells was decreased. Conclusion. DN golden hamster kidney NLRP3-Caspase-1-GSDMD signalling was enhanced. BBR can reduce oxidative stress damage by regulating antioxidative Nrf2 and then regulating NLRP3-Caspase-1-GSDMD signalling to inhibit pyroptosis, antagonizing DN inflammation-induced damage.

scholarly journals TNFR1 is Upregulated and Mediates Apoptosis in Cumulus Cells of Women With Polycystic Ovarian Syndrome

2021 ◽  
Author(s):  
Yaping Jiang ◽  
Rui Jiang ◽  
Peng Zhang ◽  
qiong Yu ◽  
Hongping Ba ◽  
...  
Keyword(s):  
Polycystic Ovary Syndrome ◽  
Signaling Pathway ◽  
Granulosa Cells ◽  
Follicular Fluid ◽  
Polycystic Ovary ◽  
Cumulus Cells ◽  
Control Group ◽  
Ovary Syndrome ◽  
Tnf Α ◽  
Pcos Group

Abstract Purpose To investigate the changes of human granulosa cell, TNFR1, TNFR2 and their downstream molecules in patients with polycystic ovary syndrome (PCOS) and the control group. Methods We recruited infertile women with polycystic ovary syndrome (n = 30) and compared them with infertility due to fallopian tube obstruction(n = 30, control group). The ovaries were stimulated with GnRH agonists and gonadotropins. Follicular fluid from large follicles ([14 mm]) was pooled and granulosa cells (GCs) were separated by a cellular filter. The TNF-α level of follicular fluid was measured by ELISA. TUNEL assay were used to detect the apoptosis of purified GCs. Real-time PCR and Western blotting were used to detect the expression of TNF-related signaling molecules in GCs. Results The rate of high quality embryos in the PCOS group was lower than that in the control group. There were higher percentages of apoptosis in GCs of PCOS patients than in the control group. TNF-α is upregulated in follicular fluid of PCOS patients. TNFR1 and caspase-3 mRNA level were signifificantly higher in PCOS group than in the control group. TNF-α-mediated apoptosis of PCOS granulosa cells was mainly dependent on TNFR1.The TNF-α/TNFR1 signaling pathway mediates apoptosis rather than survival in cumulus cells of PCOS patients. Conclusions TNF-α expression was upregulated in follicular fluid of PCOS patients, and TNFR1 overexpression in female granulosa cells of PCOS was associated with higher levels of apoptosis in these cells, suggesting that the TNF-α/TNFR1 signaling pathway may be a candidate for higher apoptosis in female granulosa cells of PCOS.

scholarly journals Electroacupuncture Improves Synaptic Function in SAMP8 Mice Probably via Inhibition of the AMPK/eEF2K/eEF2 Signaling Pathway

2019 ◽  
Vol 2019 ◽  
pp. 1-10 ◽  
Author(s):  
Weiguo Dong ◽  
Wendan Yang ◽  
Feifei Li ◽  
Wanqing Guo ◽  
Changhui Qian ◽  
...  
Keyword(s):  
Signaling Pathway ◽  
Elongation Factor ◽  
Synaptic Function ◽  
Control Group ◽  
Synaptic Loss ◽  
Elongation Factor 2 ◽  
Eukaryotic Elongation Factor 2 ◽  
Eukaryotic Elongation Factor ◽  
Samp8 Mice ◽  
Senescence Accelerated Mouse

Synaptic loss and dysfunction is associated with cognitive impairment in Alzheimer’s disease (AD). Recent evidence indicates that the AMP-activated protein kinase (AMPK)/eukaryotic elongation factor-2 kinase (eEF2K)/eukaryotic elongation factor-2 (eEF2) pathway was implicated in synaptic plasticity in AD. Therapeutic strategies for AD treatment are currently limited. Here, we investigate the effects of electroacupuncture (EA) on synaptic function and the AMPK/eEF2K/eEF2 signaling pathway in male senescence-accelerated mouse-prone 8 (SAMP8) mice. Male 7-month-old SAMP8 and SAMR1 mice (senescence-accelerated mouse resistant 1) were randomly divided into 3 groups: SAMR1 control group (Rc), SAMP8 control group (Pc), and SAMP8 electroacupuncture group (Pe). The Pe group was treated with EA for 30 days. Transmission electron microscopy (TEM) was used to observe the structure of synapse. The protein and mRNA expression of synaptophysin (SYN) and postsynaptic density 95 (PSD95) was examined by immunohistochemistry, western blot, and real-time RT-PCR. The activity of AMPK and eEF2K was studied by western blot. Our results showed that EA ameliorated synaptic loss, increased the expression of SYN and PSD95, and inhibited AMPK activation and eEF2K activity. Collectively, these findings suggested that the mechanisms of EA improving synaptic function in AD may be associated with the inhibition of the AMPK/eEF2K/eEF2 signaling pathway.

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