Motion sickness (MS) is an acute disorder that occurs in healthy individuals worldwide regardless of gender, age, or ethnicity. Our study used a mouse model to rule out the effects of any psychological factors related to MS and EA. Subjects were randomly separated into four groups, namely the control group (Con), motion sickness inducing group (MS), mentioning sickness inducing with electroacupuncture treatment group (EA) and motion sickness inducing only in TRPV1 knockout mice group (TRPV1−/−). The consumption of kaolin, a non-nutrient substance, was measured as a behavior observed response of an emetic reflex in a murine model. This behavior is referred to as pica behavior. Our results showed that pica behavior was observed in the MS group. Moreover, kaolin consumption in the EA group decreased to the average baseline of the control group. A similar result was observed in TRPV1 null mice. We also observed an increase of TRPV1 and related molecules in the thalamus, hypothalamic and brain stem after MS stimulation and a significant decrease in the EA and TRPV1 null groups. This is the first study to demonstrate that TRPV1 pathways are possibly associated with mechanisms of MS, and can be attended through EA or TRPV1 genetic manipulation.

Inflammatory pain sensation is an important symptom which protects the body against additional tissue damage and promotes healing. Discovering long-term and effective treatments for pain remains crucial in providing efficient healthcare. Electroacupuncture (EA) is a successful therapy used for pain relief. We aimed to investigate effects and mechanisms of Complete Freund’s Adjuvant (CFA)-inducing inflammatory pain in the cerebellum, and the inhibition of this inflammatory hyperalgesia using EA at Zusanli acupoint (ST36). The results display a significant increase in mechanical and thermal sensitivities in the CFA and CFA + SHAM groups, which was significantly reduced in the CFA+EA and CFA + KO groups. This evidence was substantiated in the protein levels observed using immunoblotting, and presented with significant escalations after CFA inducing inflammatory hyperalgesia in CFA and CFA + SHAM groups. Then, they were significantly attenuated by EA in the CFA + EA group. Furthermore, the CFA + transient receptor vanilloid member 1 (TRPV1)−/− group indicated similar significant decreases of protein expression. Additionally, a concomitant overexpression in lobule VIa was also observed in immunofluorescence. These consequences suggest that CFA-induced inflammatory pain provokes modifications in cerebellum lobules V, VIa and VII, which can subsequently be regulated by EA treatment at the ST36 through its action on TRPV1 and related molecular pathways.

Obesity is a global health problem affecting the general population. Acupoint catgut embedding (AcE) is an alternative treatment that involves the implantation of absorbable catgut suture at acupoints. The transient receptor vanilloid member 1 (TRPV1) is a calcium ion channel that responds to several chemical ligands and is identified in numerous locations throughout the body. The aim of the present study was to examine the effect of AcE treatment on obesity and its associated complications through various neural mechanisms in a murine model. A c57/BL6 wild type (WT) and TRPV1-/-(KO) mouse model was utilized to exclude any psychological factors associated with obesity. The WT-HFd-AcE and WT-HFd-SHAM groups received weekly AcE or placebo treatments at the bilateral ST36 acupoint. The mice were fed with a normal mice chow diet (Nd) or a high-fat food diet (HFd; 45 kcal%), and their body weights were recorded once a week. After 8 weeks, the subjects were sacrificed and changes in the levels of a number of biomarkers were investigated using ELISA, immunoblotting and immunofluorescence. The results indicated a significant decrease in body weight variation for the WT-HFd-AcE group compared with the WT-HFd and WT-HFd-SHAM groups, using the WT-Nd group as the body weight baseline. By contrast, KO mice fed with Nd or HFd demonstrated notable body weight maintenance throughout the experimental period. Similar patterns were observed in adipose tissue mass, glucose, leptin and insulin plasma levels, and protein molecule density of TRPV1 and its associated molecules in the hypothalamus and nucleus tractus solitarii. In contrast, in the prefrontal cortex, significant decreases in the concentrations of MAPK pathway proteins in the WT-HFd and WT-HFd-SHAM groups were observed. The levels of these proteins were significantly increased in the WT-HFd-AcE and KO-HFd groups. These results suggested that TRPV1 and its associated pathways may be involved in body weight maintenance, and may be controlled through AcE treatment or genetic manipulation.