BACKGROUND: Intervertebral disc degeneration (IVDD), a key contributor to degenerative spinal diseases such as cervical spondylosis, significantly influences the quality of life of patients. Tuina, historically employed in the clinical management of cervical spondylosis, has demonstrated positive therapeutic outcomes; however, the mechanism of Tuina remains unclear. OBJECTIVE: This study examined the efficacy of Tuina in correcting the imbalanced structure of the cervical spine and its impact on apoptotic chondrocytes within the cervical disc. The underlying mechanisms were explored using a rabbit model of IVDD induced by dynamic and static imbalances. METHODS: The IVDD rabbit model was established by restraining the head in a downward position for 12 weeks (Model group). In the Tuina1 group, treatment was performed on the posterior cervical trapezius muscle daily for 2 weeks, whereas in the Tuina2 group, treatment was performed on both the posterior cervical trapezius and anterior sternocleidomastoid muscles daily for 2 weeks. After treatment, X-ray, micro-computed tomography (CT), histological staining, qRT-PCR, and western blotting were used to evaluate the mechanism by which Tuina inhibits chondrocyte apoptosis. RESULTS: The results demonstrated that Tuina treatment inhibited chondrocyte apoptosis in cervical discs by adjusting the neck structure balance, and a more significant therapeutic effect was observed in the Tuina2 group. Lateral cervical spine X-ray and CT scans in rabbits revealed notable improvements in cervical spine curvature and vertebral structure in the treatment groups compared with those in the Model group. Hematoxylin and eosin staining and TUNEL staining further confirmed the positive impact of Tuina treatment on intervertebral disc tissue morphology and chondrocyte apoptosis. Additionally, western blotting and immunohistochemical analysis showed that Tuina treatment suppressed chondrocyte apoptosis by downregulating Bax and caspase-3 while upregulating Bcl-2. Western blotting results further indicated that Tuina could activate the FAK/PI3K/Akt signaling pathway by mediating integrin-ß1. CONCLUSION: Tuina treatment inhibited chondrocyte apoptosis in cervical discs by activating the FAK/PI3K/Akt signaling pathway, providing convincing evidence to support Tuina treatment as a promising method for IVDD.
BACKGROUND: In the domain of functional gastrointestinal disorders, Functional Dyspepsia (FD) stands out due to its widespread occurrence internationally. Historically, electroacupuncture (EA) has been employed as a therapeutic modality for FD, demonstrating notable clinical efficacy. OBJECTIVES: This research aimed to delve into the impact of EA on stress responses, minor duodenal inflammatory processes, and the integrity of the intestinal barrier within FD-affected rodent models while also elucidating the underlying mechanisms. METHODS: Thirty-six male Wistar rats were evenly distributed into three cohorts: a normal, a modeled FD, and an EA treatment group. The FD condition in the rats, barring those in the normal, was induced through a series of multifactorial procedures. For the EA cohort, the rats received electroacupuncture at the acupoints RN12 (Zhongwan) and ST36 (Zusanli) for 20 minutes daily over a span of one week. The gastric residue rate (GRR), intestinal propulsion rate (IPR), and changes in emotional state were measured in each group of rats. Additionally, serum levels of corticotropin-releasing hormone (CRH), adrenocorticotropic hormone (ACTH), and corticosterone (CORT) were detected, and the duodenal inflammatory condition and intestinal mucosal barrier status were observed through staining and fluorescence. The expression levels of Claudin-1, Junctional Adhesion Molecule 1 (JAM-1), Corticotropin-Releasing Factor (CRF), and Corticotropin-Releasing Factor Receptor 1 (CRF-R1) were also detected. RESULTS: The study demonstrated that EA had a positive effect on body weight and food intake, GRR, and IPR in FD rats. Additionally, the EA group showed a decrease in serum levels of CRH, ACTH, and CORT, as well as a decrease in the number of duodenal mast cells and tryptase content. Furthermore, the expression of tight junction proteins Claudin-1 and JAM-1 was increased in the EA group compared to the model group. EA also reduced the levels of CRF and CRF-R1 in the hypothalamus and duodenum. CONCLUSION: EA has been shown to improve the stress state of FD rats, inhibit the activation of mast cells in the duodenum, and reduce low-grade inflammatory response and damage to the intestinal mucosal barrier. It is believed that EA achieves these effects by modulating the expression of CRF and its receptors in the brain-gut interaction pathway through the CRF signaling pathway. This provides a new approach to treating FD.
