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

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.

A Mechanism for the Treatment of Cardiovascular and Renal Disease: TRPV1 and TRPA1

“…TRPV1 is a member of the TRP ion channel vanilloid receptor subtype family and is a good nonselective cation channel. 24 TRPV1 is expressed in the trigeminal ganglia, dorsal root ganglia, neurons, adipocytes, smooth muscle cells, endothelial cells, and renal cells. 25 In addition, TRPV1 is capable of promoting a variety of pathophysiological states in the respiratory, cardiovascular, metabolic, and renal systems, 26 leading to the release of sensory neuropeptides, such as calcitonin gene–related peptide (CGRP) and substance P (SP), from the corresponding nerve endings after stimulation by injurious stimuli, such as heat, acid, ischemia, hypoxia, and stress, or agonized by its specific agonist capsaicin.…”