scholarly journals Correction: Fangjing decoction relieves febrile seizure-induced hippocampal neuron apoptosis in rats via regulating the Akt/mTOR pathway

2019 ◽  
Vol 39 (1) ◽  
Keyword(s):  
Febrile Seizure ◽  
Hippocampal Neuron ◽  
Mtor Pathway ◽  
Neuron Apoptosis

scholarly journals Fangjing decoction relieves febrile seizures-induced hippocampal neuron apoptosis in rats via regulating the Akt/mTOR pathway

2018 ◽  
Vol 38 (5) ◽  
Author(s):  
Xian-ke Xu ◽  
Sun-yao Wang ◽  
Ying Chen ◽  
Lu Zhan ◽  
Zheng-yang Shao ◽  
...  
Keyword(s):  
Hippocampal Neurons ◽  
Hippocampal Neuron ◽  
Febrile Seizures ◽  
Mtor Pathway ◽  
Mtor Signaling ◽  
Rat Hippocampus ◽  
Control Group ◽  
Protective Effects ◽  
Bax Protein ◽  
Neuron Apoptosis

Background: Fangjing decoction is a Traditional Chinese Medicine that exhibits anticonvulsive effects in treating febrile seizures (FS). Its action mechanism and the regulation on Akt/mammalian target of rapamycin (mTOR) pathway were revealed in the present study. Methods: FS model was established in Sprague–Dawley rats with or without Fangjing decoction treatment. On day 5, following initiation of drug treatment, seizures were monitored. Hippocampal neuron apoptosis was assessed using terminal dUTP nick end-labeling method. The levels of Bax, protein kinase B (Akt), phospho-Akt (p-Akt), mTOR, and p-mTOR proteins were analyzed using Western blotting. The content of hippocampal γ-aminobutyric acid (GABA) was measured by using ELISA assay. Results: Compared with the control group (n=8), Fangjing decoction effectively shortened escape latency and duration of FS and decreased the frequency of FS in rats (n=8). Concomitantly, the apoptosis of hippocampal neurons, as well as Bax protein levels were also decreased in FS rats which were treated with Fangjing decoction. In addition, the Akt/mTOR signaling was found to be activated in rat hippocampus following FS, as evidenced by increased p-Akt and p-mTOR, while Fangjing decoction could inhibit the activation of Akt/mTOR signaling. Furthermore, the low GABA content in rat hippocampus following FS was significantly elevated by Fangjing decoction treatment. More importantly, SC79, a specific activator for Akt, apparently attenuated the protective effects of Fangjing decoction on FS rats. Conclusion: These results suggest that Fangjing decoction protects the hippocampal neurons from apoptosis by inactivating Akt/mTOR pathway, which may contribute to mitigating FS-induced brain injury.

scholarly journals Qiangji Decoction Alleviates Neurodegenerative Changes and Hippocampal Neuron Apoptosis Induced by D-Galactose via Regulating AMPK/SIRT1/NF-κB Signaling Pathway

2021 ◽  
Vol 12 ◽  
Author(s):  
Li-Ling He ◽  
Yun-Cui Wang ◽  
Ya-Ting Ai ◽  
Ling Wang ◽  
Si-Meng Gu ◽  
...  
Keyword(s):  
Neurodegenerative Diseases ◽  
Signaling Pathway ◽  
Learning And Memory ◽  
Hippocampal Neuron ◽  
Caspase 3 ◽  
Brain Aging ◽  
Tunel Staining ◽  
Nissl Staining ◽  
Memory Impairments ◽  
Neuron Apoptosis

Qiangji Decoction (QJD), a classic formula, has been widely used to treat brain aging–related neurodegenerative diseases. However, the mechanisms underlying QJD’s improvement in cognitive impairment of neurodegenerative diseases remain unclear. In this study, we employed D-galactose to establish the model of brain aging by long-term D-galactose subcutaneous injection. Next, we investigated QJD’s effect on cognitive function of the model of brain aging and the mechanisms that QJD suppressing neuroinflammation as well as improving neurodegenerative changes and hippocampal neuron apoptosis. The mice of brain aging were treated with three different dosages of QJD (12.48, 24.96, and 49.92 g/kg/d, respectively) for 4 weeks. Morris water maze was used to determine the learning and memory ability of the mice. HE staining and FJB staining were used to detect the neurodegenerative changes. Nissl staining and TUNEL staining were employed to detect the hippocampal neuron apoptosis. The contents of TNF-α, IL-1β, and IL-6 in the hippocampus were detected by using ELISA. Meanwhile, we employed immunofluorescence staining to examine the levels of GFAP and IBA1 in the hippocampus. Besides, the protein expression levels of Bcl-2, Bax, caspase-3, cleaved caspase-3, AMPKα, p-AMPKα-Thr172, SIRT1, IκBα, NF-κB p65, p-IκBα-Ser32, and p-NF-κB p65-Ser536 in the hippocampus of different groups were detected by Western blot (WB). Our findings showed that the QJD-treated groups, especially the M-QJD group, mitigated learning and memory impairments of the model of brain aging as well as the improvement of neurodegenerative changes and hippocampal neuron apoptosis. Moreover, the M-QJD markedly attenuated the neuroinflammation by regulating the AMPK/SIRT1/NF-κB signaling pathway. Taken together, QJD alleviated neurodegenerative changes and hippocampal neuron apoptosis in the model of brain aging via regulating the AMPK/SIRT1/NF-κB signaling pathway.

Action of Akt Pathway on La-Induced Hippocampal Neuron Apoptosis of Rats in the Growth Stage

2020 ◽  
Vol 38 (2) ◽  
pp. 434-446
Author(s):  
Jinting Wang ◽  
Tianwei Wu ◽  
Lan Ma ◽  
Ying Guo ◽  
Yali Huang ◽  
...  
Keyword(s):  
Hippocampal Neuron ◽  
Growth Stage ◽  
Akt Pathway ◽  
Neuron Apoptosis

scholarly journals Molecular Mechanism of ATF6α/S1P/S2P Signaling Pathway in Hippocampal Neuron Apoptosis in SPS Rats

2021 ◽  
Author(s):  
liang han ◽  
Yan hao Xu ◽  
Yu xiu Shi
Keyword(s):  
Mrna Expression ◽  
Hippocampal Neurons ◽  
Hippocampal Neuron ◽  
Control Group ◽  
Tunel Staining ◽  
Apoptosis Rate ◽  
Memory Disorder ◽  
Caspase 12 ◽  
Induced Apoptosis ◽  
Neuron Apoptosis

Abstract Apoptosis of hippocampal neurons is one of the mechanisms of hippocampal atrophy in posttraumatic stress disorder (PTSD), and it is also one of the important reasons of memory disorder in PTSD patients. The endoplasmic reticulum stress (ERS) mediated by activated transcription factor 6α(ATF6α)/site 1 protease (S1P)/S2P is involved in cell apoptosis, but it is not clear whether it is involved in hippocampal neuron apoptosis caused by PTSD. The PTSD rat model was constructed by the single-prolonged stress (SPS) method. The experiment was divided into two parts: (1) Control group, SPS 1d group, SPS 7d group, SPS 14d group. (2) Control group, SPS 7d group, SPS 7d+AEBSF group, control+AEBSF group. 4-(2-Aminoethyl) benzenesulfonyl fluoride hydrochloride (AEBSF) is an ATF6α pathway inhibitor. The expression of ATF6α, glucose regulated protein (GRP78), S1P, S2, C/EBP homologous protein (CHOP), caspase-12 protein and mRNA in the hippocampus of PTSD rats were detected by immunohistochemistry, Western blotting and qRT-PCR. The apoptosis of hippocampal neurons was detected by TUNEL staining. In experiment 1, the protein and mRNA expression of ATF6α, GRP78 increased gradually in SPS 1d group and SPS 7d group, but decreased in SPS 14d group(P<0.01). In experiment 2, compared with the control group, the protein and mRNA expression of ATF6α, GRP78, S1P, S2P, CHOP, caspase-12 and apoptosis rate were significantly increased in SPS 7d group(P<0.01). However, the protein and mRNA expression of ATF6α, GRP78, S1P, S2P, CHOP, caspase-12 and apoptosis rate were significantly decreased after AEBSF pretreatment(P<0.01). SPS induces apoptosis of hippocampal neurons by activating ERS mediated by ATF6α, suggesting that ERS-induced apoptosis is involved in the occurrence of PTSD.

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