Stimulated by Liu et al 2023.[1]
EA – electroacupuncture
key to acronyms
IBS – irritable bowel syndrome
UC – ulcerative colitis
DSS – dextran sodium sulphate
DEGs – differentially expressed genes
GSEA – gene set enrichment analysis
This paper came up in one of my searches in the last week and I filed it for consideration. It made the cut because a colleague sent it to me for my opinion. She thought it seemed rather sure of itself in claiming efficacy in IBS.
Scientific Reports is a well-known open access journal within the Nature portfolio of 181 journals. It publishes peer reviewed research from the natural sciences, psychology, medicine, and engineering. It has an impact factor of just under 5 and is the 5th most cited journal in the world with 696 000 citations in 2021.
The paper is a laboratory study focussing on intestinal barrier function in two different diseases and the effect of EA at ST36 on these aspects of the conditions. It uses well-established rodent models for IBS and UC. The former involves instilling acetic acid into the colon every other day for a week and the latter is produced by drinking DSS water for 7 days.
The intestinal barrier can be divided into 3 different layers: the mucus barrier; the epithelial barrier; and the vascular barrier. This paper reports on the different abnormalities in the intestinal barrier of the IBS and UC mouse models and how these were affected by EA at ST36 using transcriptome data analysis.
The transcriptome is essentially the RNA sequences found in the relevant cells. In this case the cells of the colon were used. The quantity of individual RNA sequences reflect the degree to which genes are either upregulated or down regulated and therefore the degree to which certain proteins are enhanced or diminished. These proteins could be inflammatory mediators, secretory components related to the mucus barrier, cellular components of tight junctions or proteins related to the vascular barrier.
The UC model induced more changes in the transcriptome with 3095 DEGs compared with only 183 DEGs in the IBS model. This is nicely illustrated in the volcano plots in the image above. The most significant changes in the UC mice related to inflammatory-related genes, while those in the IBS mice were actin-related genes that are involved in cell movement. Inflammatory and immune pathways were enhanced to a greater degree in UC compared with IBS mice. In regard to the intestinal barrier, there were differences noted in all three layers between the models.
GSEA demonstrated changes related to the mucus barrier, with increased extracellular matrix and secretory granules and reduced regulation of secretion by the cell in UC mice. Whereas in the IBS mice there was only negative regulation of secretory pathways and intracellular protein transport. In terms of the epithelial barrier, the US mice showed increased levels of gap junction components and negative regulation of cell adhesion, but IBS mice only showed changes in the morphology of polarised epithelial cells. The UC mice showed more changes in the vascular barrier, with negative regulation of locomotion and changes in angiogenesis and endothelial cell apoptosis. The changes in IBS mice were mainly related to vasoconstriction.
EA was applied to ST36 using pairs of needles on each side (my favoured approach) at 2Hz and 0.2mA for 30 minutes every day after induction of the models. A Hans-200 device was used and I think the pulse width of this device is 500μs, which is on the long side (I generally use ~200μs at 2Hz).
EA improved disease activity, faecal water content and gut permeability in both models as well as reducing abdominal sensitivity in the IBS mice and increasing weight in the UC mice.
The intestinal mucus barrier was improved in both models and inflammatory markers were reduced. The epithelial barrier was assessed using immunofluorescence of tight junction proteins (Zonula Occludens-1, Occludin and Claudin-1) and EA significantly improved the levels of these proteins.
The gut vascular barrier was assessed using two protein markers and mesenteric blood flow. EA normalised these markers and improved blood flow in the UC model. Mesenteric blood flow was not abnormal in the IBS model.
The authors concluded that EA at ST36 functioned as a form of homeostatic regulation. I guess this was based on the fact that some measures that increased in the models were decreased with EA and others that were decreased in the models were increased with EA and those that were not affected in the models were also not affected by EA.
This conclusion will not be a surprise to those of you familiar with the acupuncture research literature, but it is nice to have this homeostatic regulatory idea supported by the latest genomic analysis.
References
1 Liu S, Huang Q, Huang Q, et al. The protective effects of electroacupuncture on intestinal barrier lesions in IBS and UC model. Sci Rep 2023;13:7276. doi:10.1038/s41598-023-34182-z
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