Interstitial cells of Cajal (ICCs) and nNOS play a crucial role in diabetic gastrointestinal dysmotility(DGD). Our previous study found that electro-acupuncture(EA) on ear point ‘stomach’ could repair the gastric dysrhythmias in rats induced by rectal distention(RD) after meal. However, little were known about the possible effect of auricular electro-acupuncture (AEA) on diabetic rats. Thus, we designed this study to investigate the effect of AEA on streptozotocin(STZ)-induced diabetic rats. Forty male Sprague_Dawley (SD) rats were injected with STZ, at the end of 8th week after injection, animals were randomly divided into four groups and received 2 weeks-treatment(10 times) respectively: control group(CON,n = 10, no stimulation), sham auricular electro-acupuncture group(SEA,n = 10, low frequency EA on earlobes), auricular eletro-acupuncture group(AEA,n = 10, low frequency EA on ear point ‘stomach’), and ST-36 group(ST-36,n = 10, low frequency EA on ST-36). Gastrointestinal (GI) motility was measured by GI transit rate. ICCs(c-kit+ expression) in antrum were analyzed by Immunohistochemistry and western blotting. NO level in blood serum were detected by Griess Reagent, and nNOSmRNA expression in antrum were determined by Real-time PCR. GI transit rate and ICCs(c-kit+ expression) in antrum of AEA group have the tendency to increase compared with CON group, but had no statistics difference (P>0.05). nNOSmRNA expression in antrum of AEA group was dramatically increased compared with CON group (P = 0.037). Low frequency EA on ear ‘stomach’ point could significantly up-regulate nNOS mRNA expression and ameliorate the ICCs networks partly in gastric antrum of STZ -induced diabetic rats, which may has benefits on regulating the GI motility.

Background: Visceral hypersensitivity (VH) is acknowledged as a critical pathogenic mechanism underlying functional gastrointestinal disorders (FGIDs), which is influenced by dysregulation of the gut‐brain axis. Transauricular vagus nerve stimulation (taVNS) is a clinically used intervention for the relief of visceral pain; however, its underlying neural mechanisms remain poorly understood. Drawing on the pathogenesis of VH and our team's previous research, we hypothesized that taVNS mitigates VH through the nesfatin‐1/corticotropin‐releasing factor (CRF) pathway. This study aims to elucidate the potential central regulatory mechanisms that contribute to the analgesic effects of taVNS. Methods: A validated VH model was established in Sprague–Dawley (SD) rats through maternal separation (MS) combined with acetic acid enema. The VH rats underwent taVNS at frequencies of 2 Hz, 10 Hz, and 15 Hz, whereas the sham group received 2 Hz electrical stimulation at the earlobe. The visceral pain threshold was evaluated using the abdominal withdrawal reflex (AWR) scoring and electromyographic activity of the external oblique muscle. Additionally, Western blot analysis was conducted to assess the expression levels of nesfatin‐1, CRF, and its receptors 1 and 2 (CRF1/2R) in the hypothalamus. Key Results: The analyses of AWR and electromyogram (EMG) responses indicated that (a) the area under the curve (AUC) of the EMG response to colorectal distension (CRD) at four distension pressures (20, 40, 60, and 80 mmHg) was significantly elevated in the VH group. (b) The AUC was significantly reduced in the 2 Hz taVNS group across all four distension pressures. (c) The 10 Hz taVNS group exhibited a significant decrease in the AUC at 20 mmHg and 40 mmHg. Furthermore, the results of Western blot analysis demonstrated that (a) 2 Hz taVNS significantly lowered the expressions of nesfatin‐1, CRF, and CRF1R, aligning with the findings in the sham group. (b) Both 10 Hz and 15 Hz taVNS significantly decreased CRF expression, whereas nesfatin‐1 and CRF1R expression remained unchanged. (c) There was no significant downregulation of CRF2R expression among the intervention groups. Conclusion: This study demonstrated that taVNS alleviates VH, potentially via the nesfatin‐1/CRF/CRF1R signaling pathway in the rat hypothalamus. Furthermore, the analgesic effect was frequency‐dependent, with 2 Hz taVNS providing a more effective reduction in visceral pain.

Introduction Atrial fibrillation (AF) is the prevalent cardiac arrhythmia and can significantly impair the quality of life (QoL). Although catheter ablation (CA) is an established treatment for AF,post-procedural complications or perceived inadequate control of AF may diminish the QoL for some patients, potentially even to levels lower than pre-procedure. Preliminary findings from our previous pilot trial indicate that acupuncture may positively influence QoL in AF patients post-CA. This study aims to increase the sample size to evaluate the efficacy of acupuncture as an adjunctive treatment to conventional medical therapy in improving QoL of patients with AF after CA. Methods and design This multicentre randomised clinical trial will be conducted in China. A total of 146 eligible patients will be randomly assigned in a 1:1 ratio to either the acupuncture group or the sham acupuncture group. All patients will receive standard postablation care and undergo 18 sessions of acupuncture/sham acupuncture within 12 weeks following CA, followed by a 9-month follow-up period. The primary outcome is the change in the Atrial Fibrillation Effect on Quality-of-Life (AFEQT) summary score from baseline to months 6 after CA. Secondary outcomes include the changes in the AFEQT subscale scores at months 6, the AFEQT summary and subscale score at months 3 and 12, AF burden, AF recurrence, heart rate variability, number of cardioversions, repeat CA procedures, European Heart Rhythm Association score, number of arrhythmia-related hospitalisations, average heart rate, use of Six-Dimensional Health State Short Form to assess health status, costs incurred by disease treatment, Credibility/Expectancy Questionnaire and blinded assessments. Adverse events will also be meticulously recorded throughout the trial. Ethics and dissemination Ethics approval has been granted by the Ethics Committee of Beijing University of Traditional Chinese Medicine (approval no: 2020BZYLL0802) and seven other subcentres. The findings of the study results will be disseminated through presentations at scientific conferences or publications in peer-reviewed journals. Trial registration number ChiCTR2100049323.

Diabetes mellitus is a prevalent chronic condition globally. A frequent complication is gastric motility disorder, which substantially impacts patients' quality of life and overall well-being. The SMC-ICC-PDGFRα⁺ (SIP) syncytium plays an important role in coordinating gastrointestinal (GI) motility. Auricular vagus nerve stimulation (aVNS) has demonstrated promising therapeutic efficacy against diabetic motility disorders, yet the underlying mechanism is not well understood. This study aims to evaluate whether low-frequency aVNS attenuates gastric dysmotility in diabetic rats through regulation of the SIP syncytium and its signaling pathways. Male Sprague-Dawley rats were employed to induce a diabetic gastric motility disorder (DGMD) model using streptozotocin (STZ). The DGMD rats underwent treatment with aVNS, a combination of aVNS and body electroacupuncture (aVNS-EA), and sham aVNS. Gastric motility was evaluated by the solid gastric emptying rate (SGER). Gastric antrum pathology was assessed via hematoxylin and eosin (H&E) staining, SIP syncytium function was evaluated by immunofluorescence, and serum nitric oxide (NO) levels were measured with a Griess kit. Low-frequency aVNS significantly enhanced SGER and upregulated the expression of interstitial cells of Cajal (ICCs) and platelet-derived growth factor receptor alpha-positive (PDGFRα⁺) cells in the antrum; the smooth muscle marker α-SMA was increased at the immunofluorescence and messenger RNA (mRNA) levels, but not significantly at the protein level. aVNS-EA exhibited similar effects, whereas sham aVNS showed no significant change. aVNS also upregulated neuronal nitric oxide synthase (nNOS), increased NO release, and activated the soluble guanylate cyclase-cyclic guanosine monophosphate-protein kinase G1 (sGC-cGMP-PKG1) pathway. Treatment with 1H-[1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one (ODQ), the soluble guanylate cyclase (sGC) inhibitor, reversed the aVNS-induced improvements in SGER and SIP syncytium integrity. In contrast, aVNS-EA benefits were only partially inhibited by ODQ. These results suggest that low-frequency aVNS improves gastric motility and SIP syncytium function in diabetic rats by activating the NO/sGC/cyclic guanosine monophosphate (cGMP)/protein kinase G1 (PKG1) pathway and that the aVNS-EA yields additional beneficial effects.