Governor Vessel Moxibustion Therapy Improves Microbiota Structure in Ankylosing Spondylitis Patients

Background. Clinical studies have shown that ankylosing spondylitis (AS) could be significantly improved by Governor Vessel moxibustion (GVM) therapy. Objective. Study whether GVM therapy alleviates the clinical symptoms of AS by modulating intestinal microbiota. Methods. A total of 9 AS patients and 9 paired healthy individuals were enrolled, and GVM therapy was provided to the AS patients. Stool, urine, and saliva samples from the healthy individuals and the AS patients before and after GVM therapy were collected, and 16S rRNA gene sequencing was performed for microbiota analysis. Results. We found that GVM therapy can significantly alleviate the symptoms of AS, such as diarrhea, abdominal pain, and bloating. GVM therapy also decreased the abundances of Bacteroides and Prevotella while increasing the abundances of beneficial bacteria, such as Lactobacillus, in the gut microbiota of the AS patients. The analyses for AS clinical data and microbial abundances in AS patients revealed their multiple significant correlations ( P < 0.01 ); for example, an unclassified crystal was positively correlated with AF12 and Delftia, monocyte had a negative correlation with Scardovia, and human leukocyte antigen-B27 was negatively correlated with Catenibacterium, Coprococcus, and Oscillospira. Conclusions. Overall, these findings demonstrate that GVM therapy can alleviate AS clinical symptoms, and at the same time, it improves the microbial structure of microbiota in AS patients. This trial is registered with Chinese Clinical Trial Registry ChiCTR2100051907.

Electroacupuncture at Governor Vessel improves neurobehavioral function via silencing complexin I

Governor Vessel electro-acupuncture (GV), as a traditional Chinese medicine, has been proved that it can reduce scar and promote axon regeneration. However, the underlying mechanism remains unclear. Herein, complexin I (CPLX1), as a candidate protein involved in the process of GV treatment on spinal cord contusion (SCC), was found by using protein chip. Therefore, using a CRISPR/Cas9 knockout approach, we silenced CPLX1 to assess its role in the process of GV treatment. Additionally, eIF5A1 promotes translation of CPLX1 with PPG sequence, we attempt to uncover whether eIF5A1 play a role in GV treatment. Indeed, GV can reduce scar and promote axon regeneration after SCC. CPLX1-/+ SCC rats demonstrated that decreased CPLX1 improved the microenvironment of injured area via reducing the components of fibrotic scar and further enhanced the synaptic plasticity, which benefit the regeneration of axons. And eIF5A1 could regulate the expression of CPLX1 in the process of GV treatment. Therefore, GV contributes to axon regeneration and synapse plasticity via eIF5A1 regulating CPLX1 following SCC, providing a convincible mechanism for improving the therapeutic efficacy of GV for SCC.

Electroacupuncture at Governor Vessel improves neurobehavioral function via reduction of complexin1

Electroacupuncture at Governor Vessel (GV), as a traditional chinese medicine, has been proved that it can reduce scar and promote axon regeneration. However, the underlying mechanism remains unclear. Herein, complexin1 (CPLX1), as a candidate protein, was found using protein chip. Therefore, using a CRISPR/Cas9 knockout approach, we deleted CPLX1 specifically in the SD rats to assess the role of CPLX1 in GV treatment. Additionally, eIF5A1 stimulate the translation of CPLX1 with PPG sequence, we attempt to uncover whether eIF5A1 play a role in the GV treatment. In fact, GV can reduce scar and promote axon regeneration after SCC. CPLX1−/+ SCC rats demonstrated that decreased CPLX1 improved the microenvironment of injured area via reducing the components of fibrotic scar and further enhanced the synaptic plasticity, which benefit the regeneration of axons. And eIF5A1 could regulate the expression of CPLX1 in the process of GV treatment. Therefore, GV contributes to axon regeneration and synapse plasticity via eIF5A1 regulating CPLX1 following SCC, providing a convincible mechanism for improving the therapeutic efficacy of GV for SCC.