Abstract
BackgroundElectroacupuncture (EA) stimulation has been shown to have a great therapeutic potential for treating gastrointestinal motility disorders. However, no evidence has clarified the mechanisms contributing to the effects of EA stimulation at the Zusanli acupoint (ST.36). This study was designed to investigate the regulative effect of EA stimulation at the ST.36 on gastric motility and to explore its possible mechanisms.MethodsThirty Sprague-Dawley rats were randomly divided into three groups: the ST.36 group, the non-acupoint group, and the control group. EA stimulation was set at 2 Hz, continuous mode, and 1 V for 30 min. The frequency and average peak amplitude of gastric motility were measured by electrogastrography. The protein kinase C (PKC) and mitogen-activated protein kinase (MAPK) signaling pathways were assessed using real-time polymerase chain reactions. Caldesmon (CaD) and calponin (CaP) protein expression in the gastric antrum were detected on Western blots. A Computed Video Processing System was used to evaluate morphological changes in smooth muscle cells (SMCs) from the gastric antrum.ResultsEA stimulation at ST.36 had a dual effect on the frequency and average peak amplitude. Additionally, EA stimulation at ST.36 regulated the expression of some genes in the PKC and MAPK signaling pathways, and it regulated the expression of the CaD and CaP proteins. EA serum induced SMC contractility. Promotion of gastric motility may correlate with up-regulation of MAPK6 (ERK3), MAPK13, and Prostaglandin-endoperoxide synthase 2 (PTGS2) gene expression, and the down-regulation of the collagen, type I, alpha 1 (COL1A1) gene and CaD and CaP protein expression. Inhibition of gastric motility may correlate with down-regulation of the Interleukin-1 receptor type 2 (IL1R2) and Matrix metalloproteinase-9 (MMP9) genes, and up-regulation of CaD and CaP protein expression.ConclusionsEA stimulation at ST.36 regulated gastric motility, and the effects were both promoting and inhibiting in rats. The possible mechanisms may correlate with the PKC and MAPK signal transduction pathways.
Highlights
Electroacupuncture (EA) stimulation has been shown to have a great therapeutic potential for treating gastrointestinal motility disorders
Effects of EA on gastric motility EA at ST.36 produced significant changes in the absolute value of the average peak amplitude and frequency compared with the control or non-acupoint groups (P < 0.01)
The present study demonstrated that EA stimulation at ST.36 had a regulative effect on gastric motility in rats that was either stimulatory or inhibitory
Summary
Electroacupuncture (EA) stimulation has been shown to have a great therapeutic potential for treating gastrointestinal motility disorders. This study was designed to investigate the regulative effect of EA stimulation at the ST. on gastric motility and to explore its possible mechanisms. The regulation of gastrointestinal motility is complicated and involves the contraction of smooth muscle cells (SMCs). There is accumulating evidence for a secondary pathway in the regulation of smooth muscle contraction that is PKC dependent, and this pathway may be mediated by CaP and CaD activation [6,7,8,9]. Mitogen-activated protein kinase (MAPK) signaling pathways have been implicated in SMC contraction [10]. CaP may facilitate ERKdependent signaling, playing a significant role in the regulation of SMC contraction [12]
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