Electroacupuncture improves cognitive impairment in diabetic cognitive dysfunction rats by regulating the mitochondrial autophagy pathway

Ge, Xia; Cui, Qianqian; Yan, Hongli; Wang, Zhongbao; Ye, Shandong; Zhang, Qingping; Fei, Aihua

doi:10.1186/s12576-022-00854-0

Cited by 7 publications

(3 citation statements)

References 41 publications

(43 reference statements)

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“…Currently, there is no effective drug to treat diabetes-related cognitive impairment. Electroacupuncture shows good therapeutic effect on cognitive impairment ( 26 ). Our results reveal that electroacupuncture can improve the learning and memory function of diabetic mice by reducing ERS, inhibiting JNK expression and removing Aβ and Tau from hippocampal neuron cells.…”

Section: Discussionmentioning

confidence: 99%

“Adjust Zang and arouse spirit” electroacupuncture ameliorates cognitive impairment by reducing endoplasmic reticulum stress in db/db mice

et al. 2023

Front. Endocrinol.

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IntroductionDiabetic cognitive impairment (DCI) is a chronic complication of the central nervous system (CNS) caused by diabetes that affects learning and memory capacities over time. Recently, acupuncture has been shown to improve cognitive impairment in streptozotocin-induced diabetic rats. However, the effects of electroacupuncture on DCI and its underlying mechanism have not yet been elucidated in detail. MethodsIn this study, we used db/db mice as DCI animal models which showed low cognitive, learning and memory functions. Electroacupuncture significantly ameliorated DCI, which is reflected by better spatial learning and memory function using behavioral tests. The db/db mice with cognitive impairment were randomly divided into a model group (Mod) and an electroacupuncture treatment group (Acup), while db/m mice were used as a normal control group (Con). First, the mice were subjected to behavioural tests using the Morris water maze (MWM), and body weight, blood glucose, insulin, triglycerides (TG) and total cholesterol (TC) were observed; HE, Nissl, and TUNEL staining were used to observe the morphological changes and neuronal apoptosis in the mice hippocampus; Finally, Western blot and rt-PCR were applied to detect the essential proteins and mRNA of ERS and insulin signalling pathway, as well as the expression levels of Tau and Aβ.ResultsElectroacupuncture significantly ameliorated DCI, which is reflected by better spatial learning and memory function using behavioral tests. Moreover, electroacupuncture attenuated diabetes-induced morphological structure change, neuronal apoptosis in the hippocampus of db/db mice. Our results revealed that electroacupuncture could regulate the expression levels of Tau and Aβ by improving hippocampal ERS levels in db/db mice, inhibiting JNK activation, attenuating IRS1 serine phosphorylation, and restoring normal transduction of the insulin signaling pathway.DiscussionIn summary, ERS and insulin signaling pathway paly causal roles in DCI development. Electroacupuncture can significantly alleviate the pathogenesis of DCI, improve mice's learning and memory ability, and improve cognitive dysfunction. This study adds to our understanding of the effect of acupuncture on DCI and opens the door to further research on DCI.

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Section: Discussionmentioning

confidence: 99%

“Adjust Zang and arouse spirit” electroacupuncture ameliorates cognitive impairment by reducing endoplasmic reticulum stress in db/db mice

et al. 2023

Front. Endocrinol.

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“… 47 Mitophagy and structural changes of mitochondria are the main causes of neuronal dysfunction. 48 Ge et al 49 established a diabetic model of adult SD rats by using streptozotocin (STZ) have shown that electroacupuncture promotes mitophagy and improves the learning and memory function of rats by increasing the expression of Disrupted-in-Schizophrenia 1 (DISC1). The down-regulation of DISC1 leads to mitochondrial dysfunction and synaptic plasticity, resulting in cognitive impairment.…”

Section: Regulate Mitophagymentioning

confidence: 99%

Targeting Mitochondrial Homeostasis: The Role of Acupuncture in Depression Treatment

Chen¹,

Wu²,

Lv³

et al. 2023

NDT

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Background: Depression is a common mental health disorder characterized by persistent feelings of sadness, loss of interest or pleasure, and a range of physical and cognitive symptoms. It affects people of all ages and can significantly impact their daily functioning and quality of life. Mitochondrial homeostasis plays an important role in the pathogenesis of depression. Mitochondrial homeostasis includes mitophagy, mitochondrial oxidative stress, mitoptosis, mitochondrial biogenesis, and mitochondrial dynamics. The regulation of mitochondrial homeostasis is the key link in the prevention and treatment of depression. Methods: In this article, we focus on the core link of depression-mitochondrial homeostasis and summarize the research progress of acupuncture targeting mitochondrial homeostasis in the treatment of depression in recent years, so as to provide ideas and experimental basis for the research and formulation of more appropriate depression treatment strategies. Results: Acupuncture has been found to regulate mitochondrial homeostasis (by modulating mitochondrial autophagy, reducing mitochondrial oxidative stress, inhibiting mitochondrial fission, inducing mitochondrial biogenesis, and maintaining mitochondrial dynamics), alleviate depression-like behavior, and regulate signal pathways and key proteins. Conclusion: Here, we highlight the role of acupuncture in the treatment of depression. A comprehensive exploration of the impact of acupuncture on mitochondrial homeostasis could potentially present a novel mechanism for treating depression and offer fresh perspectives for the treatment of patients with clinical depression.

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“…Autophagy dysfunction is one of the major pathological hallmarks of neurodegenerative disease-associated CI [ 20 ]. Interestingly, studies demonstrated that enhanced mitophagy in damaged hippocampal neurons is conducive to improving cognitive dysfunction in rats [ 21 ]. In this context, the effect of NTRK1 on mitophagy in neurons has not been elucidated.…”

Section: Introductionmentioning

confidence: 99%

NTRK1 knockdown induces mouse cognitive impairment and hippocampal neuronal damage through mitophagy suppression via inactivating the AMPK/ULK1/FUNDC1 pathway

Yang,

Wu,

et al. 2023

Cell Death Discov.

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Hippocampal neuronal damage may induce cognitive impairment. Neurotrophic tyrosine kinase receptor 1 (NTRK1) reportedly regulates neuronal damage, although the underlying mechanism remains unclear. The present study aimed to investigate the role of NTRK1 in mouse hippocampal neuronal damage and the specific mechanism. A mouse NTRK1-knockdown model was established and subjected to pre-treatment with BAY-3827, followed by a behavioral test, Nissl staining, and NeuN immunofluorescence (IF) staining to evaluate the cognitive impairment and hippocampal neuronal damage. Next, an in vitro analysis was conducted using the CCK-8 assay, TUNEL assay, NeuN IF staining, DCFH-DA staining, JC-1 staining, ATP content test, mRFP-eGFP-LC3 assay, and LC3-II IF staining to elucidate the effect of NTRK1 on mouse hippocampal neuronal activity, apoptosis, damage, mitochondrial function, and autophagy. Subsequently, rescue experiments were performed by subjecting the NTRK1-knockdown neurons to pre-treatment with O304 and Rapamycin. The AMPK/ULK1/FUNDC1 pathway activity and mitophagy were detected using western blotting (WB) analysis. Resultantly, in vivo analysis revealed that NTRK1 knockdown induced mouse cognitive impairment and hippocampal tissue damage, in addition to inactivating the AMPK/ULK1/FUNDC1 pathway activity and mitophagy in the hippocampal tissues of mice. The treatment with BAY-3827 exacerbated the mouse depressive-like behavior induced by NTRK1 knockdown. The results of in vitro analysis indicated that NTRK1 knockdown attenuated viability, NeuN expression, ATP production, mitochondrial membrane potential, and mitophagy, while enhancing apoptosis and ROS production in mouse hippocampal neurons. Conversely, pre-treatment with O304 and rapamycin abrogated the suppression of mitophagy and the promotion of neuronal damage induced upon NTRK1 silencing. Conclusively, NTRK1 knockdown induces mouse hippocampal neuronal damage through the suppression of mitophagy via inactivating the AMPK/ULK1/FUNDC1 pathway. This finding would provide insight leading to the development of novel strategies for the treatment of cognitive impairment induced due to hippocampal neuronal damage.

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Electroacupuncture improves cognitive impairment in diabetic cognitive dysfunction rats by regulating the mitochondrial autophagy pathway

Cited by 7 publications

References 41 publications

“Adjust Zang and arouse spirit” electroacupuncture ameliorates cognitive impairment by reducing endoplasmic reticulum stress in db/db mice

“Adjust Zang and arouse spirit” electroacupuncture ameliorates cognitive impairment by reducing endoplasmic reticulum stress in db/db mice

Targeting Mitochondrial Homeostasis: The Role of Acupuncture in Depression Treatment

NTRK1 knockdown induces mouse cognitive impairment and hippocampal neuronal damage through mitophagy suppression via inactivating the AMPK/ULK1/FUNDC1 pathway

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