Abstract
Background
Electroacupuncture (EA) at Zusanli (ST36) is an alternative treatment for several
gastrointestinal motility disorders; however, the exact mechanism is unconfirmed.
We aimed to show the potential effects of EA on muscularis macrophages (MMφ), the
bone morphogenetic protein (BMP)/BMP receptor (BMPR)-Smad signal pathway, and enteric
neurons in diabetic mice. This may provide fresh insight into ways EA affects gastrointestinal
motility.
Materials and Methods
C57BL/6J healthy adult male mice were randomly divided into five groups: regular control
group, diabetes group, diabetes with sham EA group (acupuncture only), diabetes with
low-frequency EA group (10 Hz), diabetes with high-frequency EA group (HEA) (100 Hz).
The stimulation lasted eight weeks. Gastrointestinal motility was assessed. We identified
M2-like MMφ in the layer of colonic muscle by flow cytometry. Western Blot, real-time
polymerase chain reaction, and immunofluorescent staining were also used to determine
the MMφ, molecules in the BMP2/BMPR-Smad pathway, and PGP9.5, neuronal nitric oxide
synthase (nNOS) expression of enteric neurons in the colon of each group.
Results
1) HEA improved the gastrointestinal motility (gastrointestinal transit time, defecation
frequency) of diabetic mice. 2) HEA reversed the decreased proportion of M2-like MMφ
and expression of the CD206 in the colon of diabetic mice. 3) HEA restored the downregulations
of BMP2, BMPR1b, and Smad1 in the BMP2/BMPR-Smad pathway and increased downstream
enteric neurons marked by PGP9.5, nNOS in the colon of diabetes mice.
Conclusions
HEA might promote gut dynamics by upregulating M2-like MMφ in the colon of diabetic
mice, which in turn leads to the accumulation of molecules in the BMP2/BMPR-Smad signaling
pathway and downstream enteric neurons.
Keywords
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Article info
Publication history
Published online: May 26, 2023
Accepted:
March 29,
2023
Received in revised form:
March 13,
2023
Received:
January 2,
2023
Publication stage
In Press Corrected ProofFootnotes
Source(s) of financial support: The work was supported by grants from the National Natural Science Foundation of China (Number 81770536; Number 82270583).
Conflict of Interest: The authors reported no conflict of interest.
Identification
Copyright
© 2023 International Neuromodulation Society. Published by Elsevier Inc. All rights reserved.