Transcriptome Profile of Hippocampus in Rats Model of Acute Myocardial Ischemia in Response to Electroacupuncture

2020 ◽  
Author(s):  
Xin Wu ◽  
Chenkai Wang ◽  
Kun Wang ◽  
Shuai Cui ◽  
Shengbing Wu ◽  
...  

Abstract Background: Electroacupuncture (EA) alleviates acute myocardial ischemia (AMI) by regulating some brain areas, including hippocampus. The locus coeruleus (LC) is the main source of norepinephrine (NE) in the brain, including the hippocampus, and regulates cardiovascular function. The aim of the present work was to assess whether LC mediates the positive effects of EA in AMI by altering gene expression levels in the hippocampus. We addressed this in the present study by hippocampus transcriptome profiling in a rat model of AMI following EA treatment. Results: Myocardial injury markers (ischemia-modified albumin, homocysteine and lipoprotein- associated phospholipase A2) in the serum were downregulated in EA (P<0.05) compared to the M group and upregulated in E+L group (P<0.05) compared to E group. RNA sequencing analysis of the hippocampus revealed that the downregulation of 27 genes in M vs S as well as upregulation of 40 genes in M vs S were reversed by EA. These differentially expressed genes, which were validated by quantitative real-time PCR, were enriched in 20 Kyoto Encyclopedia of Genes and Genomes pathways related to glycerolipid, glycerophospholipid, and arachidonic acid metabolism as well asnervous system function (glutamatergic, cholinergic, serotonergic, GABAergic synapses). Conclusions: LC mediates the beneficial effects of EA on AMI-induced injury may be related to the observed transcriptional regulations in the hippocampus. These results provide molecular-level evidence for the therapeutic efficacy of EA in the treatment of AMI.

2002 ◽  
Vol 39 ◽  
pp. 295
Author(s):  
Banthit Khankirawatana ◽  
Suwanee Khankirawatana ◽  
John Lof ◽  
Thomas Porter

Circulation ◽  
1974 ◽  
Vol 49 (5) ◽  
pp. 943-947 ◽  
Author(s):  
RICHARD W. MYERS ◽  
ALAN S. PEARLMAN ◽  
RICHARD M. HYMAN ◽  
RICHARD A. GOLDSTEIN ◽  
KENNETH M. KENT ◽  
...  

1980 ◽  
Vol 58 (10) ◽  
pp. 777-786 ◽  
Author(s):  
David V. Godin ◽  
John M. Tuchek ◽  
Margo Moore

The molecular consequences of acute myocardial ischemia induced in rabbit hearts by ligation of the left circumflex branch of the coronary artery were assessed in terms of the biochemical properties of subcellular organelles. Mitochondrial alteration, as reflected in progressive decrease in the activity of azide-sensitive ATPase, was apparent as early as 5 min postligation, but the activity of another mitochondrial enzyme, cytochrome c oxidase, was unchanged, even following 60 min of coronary ligation. Sarcolemmal Na+,K+-ATPase exhibited a time course of inactivation similar to that of the mitochondrial ATPase, but differed from the latter in that the impairment was not reversed on reperfusion. Cellular levels of ATP, which decreased in parallel with the loss of ATPase activities, also remained depressed following reperfusion. Decreases in lysosomal enzyme latency were noted, but these occurred somewhat later than the sarcolemmal and mitochondrial alterations. Attempts to demonstrate the production of a population of labile lysosomal structures during ischemia were unsuccessful. Similarly, no alterations in the gel electrophoretic profiles of proteins or in the Pphosphatidylcholine/Pphosphatidylethanolamine ratio of isolated mitochondrial or sarcolemmal membranes from hearts subjected to ischemia and (or) subsequent reperfusion could be found. It is suggested that sarcolemmal Na+,K+-ATPase may serve as a sensitive and readily quantifiable index of irreversible cellular necrosis and, therefore, be of value in assessing the possible beneficial effects of pharmacological interventions.


Cardiology ◽  
1979 ◽  
Vol 64 (5) ◽  
pp. 265-279 ◽  
Author(s):  
Allan M. Lefer ◽  
Evan W. Polansky

2021 ◽  
Vol 12 ◽  
Author(s):  
Zhihai Huang ◽  
Yulan Zhang ◽  
Ruixue Zhou ◽  
Luodan Yang ◽  
Hongying Pan

The accumulated evidence from animal and human studies supports that exercise is beneficial to physical health. Exercise can upregulate various neurotrophic factors, activate neuroplasticity, and play a positive role in improving and enhancing cerebrovascular function. Due to its economy, convenience, and ability to prevent or ameliorate various aging-related diseases, exercise, a healthy lifestyle, is increasingly popularized by people. However, the mechanism by which exercise performs this function and how it is transmitted from muscles to the brain remains incompletely understood. Here, we review the beneficial effects of exercise with different intensities on the brain with a focus on the positive effects of lactate on neuroplasticity and cerebrovascular plasticity. Based on these recent studies, we propose that lactate, a waste previously misunderstood as a by-product of glycolysis in the past, may be a key signal molecule that regulates the beneficial adaptation of the brain caused by exercise. Importantly, we speculate that a central protective mechanism may underlie the cognitive benefits induced by exercise.


2017 ◽  
Vol 28 (3) ◽  
pp. 235-245 ◽  
Author(s):  
Carla Perrone-Capano ◽  
Floriana Volpicelli ◽  
Umberto di Porzio

AbstractMusic is a universal language, present in all human societies. It pervades the lives of most human beings and can recall memories and feelings of the past, can exert positive effects on our mood, can be strongly evocative and ignite intense emotions, and can establish or strengthen social bonds. In this review, we summarize the research and recent progress on the origins and neural substrates of human musicality as well as the changes in brain plasticity elicited by listening or performing music. Indeed, music improves performance in a number of cognitive tasks and may have beneficial effects on diseased brains. The emerging picture begins to unravel how and why particular brain circuits are affected by music. Numerous studies show that music affects emotions and mood, as it is strongly associated with the brain’s reward system. We can therefore assume that an in-depth study of the relationship between music and the brain may help to shed light on how the mind works and how the emotions arise and may improve the methods of music-based rehabilitation for people with neurological disorders. However, many facets of the mind-music connection still remain to be explored and enlightened.


1983 ◽  
Vol 106 (5) ◽  
pp. 1014-1023 ◽  
Author(s):  
Roberto Bolli ◽  
Tedd A Brandon ◽  
David J Fisher ◽  
Genaro C Fernandez ◽  
Richard R Miller

Molecules ◽  
2022 ◽  
Vol 27 (2) ◽  
pp. 341
Author(s):  
Antonia Cianciulli ◽  
Rosa Calvello ◽  
Melania Ruggiero ◽  
Maria Antonietta Panaro

Inflammaging is a term used to describe the tight relationship between low-grade chronic inflammation and aging that occurs during physiological aging in the absence of evident infection. This condition has been linked to a broad spectrum of age-related disorders in various organs including the brain. Inflammaging represents a highly significant risk factor for the development and progression of age-related conditions, including neurodegenerative diseases which are characterized by the progressive dysfunction and degeneration of neurons in the brain and peripheral nervous system. Curcumin is a widely studied polyphenol isolated from Curcuma longa with a variety of pharmacologic properties. It is well-known for its healing properties and has been extensively used in Asian medicine to treat a variety of illness conditions. The number of studies that suggest beneficial effects of curcumin on brain pathologies and age-related diseases is increasing. Curcumin is able to inhibit the formation of reactive-oxygen species and other pro-inflammatory mediators that are believed to play a pivotal role in many age-related diseases. Curcumin has been recently proposed as a potential useful remedy against neurodegenerative disorders and brain ageing. In light of this, our current review aims to discuss the potential positive effects of Curcumin on the possibility to control inflammaging emphasizing the possible modulation of inflammaging processes in neurodegenerative diseases.


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