Dynamic Changes in Brain Glucose Metabolism and Neuronal Structure in Rats with Heart Failure

Yang, Tao; Lu, Ziwen; Wang, Lei; Zhao, Yizhou; Nie, Binbin; Xu, Qing; Han, Xiao; Li, Tong; Zhao, Jiuli; Cheng, Wenkun; Wang, Baofu; Wu, Aiming; Zhu, Haiyan; Wei, Meng; Shang, Hongcai; Zhao, Mingjing

doi:10.1016/j.neuroscience.2019.10.008

Cited by 15 publications

(17 citation statements)

References 41 publications

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“…Gray matter, an important part of the central nervous system, was consisted of a large number of neuronal bodies and their dendrites. As in our previous study [27], we also found out that the number of neurons and synapses significantly decreased and Nissl bodies disappeared in HF rats. In other words, our previous studies indirectly proved the decreased gray matter density of HF patients in clinical.…”

Section: Reduction In Volumesupporting

confidence: 87%

“…In animal studies, global cognition of animals was evaluated by passive avoidance tasks, active avoidance tasks, tail suspension test, forced swim test, sucrose preference test, open field tests, long-term potentiation recording, elevated plus maze, Y-maze test, object-in-place memory task, object oddity perceptual task and Morris water maze task(n = 13) (more details shown in Table 7). The reduction of learning [23] and memory in HF animals existed in six studies, and memory impairment manifested in short-term recognition memory [24], OiP memory [25], spatial memory [10,26,27], hippocampus-dependent memory [28]. [15,20,[29][30][31].…”

Section: Obvious Cognitive Dysfunction and Depression In Hfmentioning

confidence: 99%

“…OFT Impaired hippocampus-dependent memory consolidation Down-regulation of hippocampal genes Reduced neuronal H3K4 methylation Yang, T 2020 [27] Morris water maze task Impairment of spatial memory Brain glucose metabolism of frontal cortex significantly lower in 60 days HF rats and higher in 10 days HF rats.…”

Section: Statement Of Key Findingsmentioning

confidence: 99%

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Abnormalities of hippocampus and frontal lobes in heart failure patients and animal models with cognitive impairment or depression: A systematic review

Teng

Wang

et al. 2022

PLoS ONE

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Aims This systematic review aimed to study the hippocampal and frontal changes of heart failure (HF) patients and HF animal models with cognitive impairment or depression. Methods A systematic review of the literature was conducted independently by reviewers using PubMed, Web of Science, Embase, and the Cochrane Library databases. Results and conclusions 30 studies were included, involving 17 pieces of clinical research on HF patients and 13 studies of HF animal models. In HF patients, the hippocampal injuries were shown in the reduction of volume, CBF, glucose metabolism, and gray matter, which were mainly observed in the right hippocampus. The frontal damages were only in reduced gray matter and have no difference between the right and left sides. The included HF animal model studies were generalized and demonstrated the changes in inflammation and apoptosis, synaptic reduction, and neurotransmitter disorders in the hippocampus and frontal lobes. The results of HF animal model studies complemented the clinical observations by providing potential mechanistic explanations of the changes in the hippocampus and frontal lobes.

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Section: Reduction In Volumesupporting

confidence: 87%

Section: Obvious Cognitive Dysfunction and Depression In Hfmentioning

confidence: 99%

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Abnormalities of hippocampus and frontal lobes in heart failure patients and animal models with cognitive impairment or depression: A systematic review

Teng

Wang

et al. 2022

PLoS ONE

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“…Male Sprague–Dawley rats (230–250 g) were obtained from Beijing Vital River Laboratory Animal Technology Co., Ltd. [Animal license number: SCXK (Beijing) 2016-0006]. HF after MI was induced surgically in rats by left anterior descending coronary artery (LAD) ligation as described previously ( Wu et al, 2013 ; Yang et al, 2019 ). Briefly, following anesthesia with sodium pentobarbital (40 mg/kg intraperitoneally) and intubation, a lateral thoracotomy was carried out to access the heart.…”

Section: Methodsmentioning

confidence: 99%

Qiliqiangxin Capsules Optimize Cardiac Metabolism Flexibility in Rats With Heart Failure After Myocardial Infarction

et al. 2020

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Metabolic modulation is a promising therapy for ischemic heart disease and heart failure. This study aimed to clarify the regional modulatory effect of Qiliqiangxin capsules (QLQX), a traditional Chinese medicine, on cardiac metabolic phenotypes. Sprague-Dawley rats underwent left anterior descending coronary artery ligation and were treated with QLQX and enalapril. Striking global left ventricular dysfunction and left ventricular remodeling were significantly improved by QLQX. In addition to the posterior wall, QLQX also had a unique beneficial effect on the anterior wall subject to a severe oxygen deficit. Cardiac tissues in the border and remote areas were separated for detection. QLQX enhanced the cardiac 18 F-fluorodeoxyglucose uptake and the levels and translocation of glucose transport 4 (GLUT4) in the border area. Meanwhile, it also suppressed glucose transport 1 (GLUT1) in both areas, indicating that QLQX encouraged border myocytes to use more glucose in a GLUT4-dependent manner. It was inferred that QLQX promoted a shift from glucose oxidation to anaerobic glycolysis in the border area by the augmentation of phosphorylated pyruvate dehydrogenase, pyruvate dehydrogenase kinases 4, and lactic dehydrogenase A. QLQX also upregulated the protein expression of fatty acid translocase and carnitine palmitoyl transferase-1 in the remote area to possibly normalize fatty acid (FA) uptake and oxidation similar to that in healthy hearts. QLQX protected global viable cardiomyocytes and promoted metabolic flexibility by modulating metabolic proteins regionally, indicating its potential for driving the border myocardium into an anaerobic glycolytic pathway against hypoxia injuries and urging the remote myocardium to oxidize FA to maximize energy production.

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“…A 12-lead electrocardiogram was obtained before and 2 days after the surgery. Rats were anesthetized by injecting 40 mg/kg sodium pentobarbital, and echocardiography was performed as previously described [21] . Using a Vevo 2100 Imaging System Ultrasonic Diagnostic Equipment (VisualSonics, Canada) with a real-time high-frequency scan head of 15 MHz.…”

Section: Electrocardiographic and Echocardiographic Examinationmentioning

confidence: 99%

Cognitive impairment is induced by BDNF-TrkB signaling mediating synaptic damage and reduction of amino acid neurotransmitters in heart failure rats

Wang

Teng

et al. 2023

Preprint

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Background Heart failure (HF) is often accompanied by cognitive impairment (CI). Yet, the underlying molecular mechanism is still not fully understood. Methods A HF model was prepared by ligation of the anterior descending coronary artery of the rat for 8 weeks. Echocardiography and morris water maze were performed to evaluate cardiac and cognitive function. Electron microscopy was conducted to quantify postsynaptic density (PSD) thickness, length, and cleft width of synapses. Thirteen neurotransmitters were detected by high-performance liquid chromatography, and proteins associated with the BDNF-TrkB pathway were determined by Western blot. The intervention of BDNF siRNA in fetal rat cortical neurons was chosen for further validation of the BDNF-TrkB pathway. Results HF rats passed through the original platform position in the probe trials fewer times and took more time and distance to reach the platform in the reversal phase compared with Sham rats; also, they had reduced thickness and length of PSD and increased synaptic cleft width. Expression of BDNF, TrkB, PSD95, and VGLUT1 was significantly decreased in HF rats brain. In addition, compared with Sham rats, amino acids were significantly reduced with no changes in the acetylcholine and monoamine neurotransmitters. Further examination showed that the number of synaptic bifurcation and the expression of BDNF, TrkB, PSD95, and VGLUT1 were all decreased in the neurons that interfered with BDNF-siRNA compared with those in the negative control neurons. Conclusions These data suggest that CI in HF is regulated by BDNF-TrkB signaling, mediating synaptic damage and reduction of amino acid neurotransmitters.

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Dynamic Changes in Brain Glucose Metabolism and Neuronal Structure in Rats with Heart Failure

Cited by 15 publications

References 41 publications

Abnormalities of hippocampus and frontal lobes in heart failure patients and animal models with cognitive impairment or depression: A systematic review

Abnormalities of hippocampus and frontal lobes in heart failure patients and animal models with cognitive impairment or depression: A systematic review

Qiliqiangxin Capsules Optimize Cardiac Metabolism Flexibility in Rats With Heart Failure After Myocardial Infarction

Cognitive impairment is induced by BDNF-TrkB signaling mediating synaptic damage and reduction of amino acid neurotransmitters in heart failure rats

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