Pressing Intervention Alleviates Pain in Rats With Myofascial Trigger Points via the TRPV1 Channel in Unmyelinated...

Although pressing intervention is widely used clinically to alleviate pain associated with chronic myofascial trigger points (MTrPs), the mechanisms by which it modulates pain via sensory nerves remain unclear. This study aimed to investigate the effects of pressing intervention on transient receptor potential vanilloid 1 (TRPV1) channels in sensory nerves and to explore its potential analgesic mechanisms.

Twenty-six male Sprague-Dawley rats were randomly divided into a blank group (n = 6) and a model establishment group (n = 20). Chronic MTrPs were induced in the model group by blunt strike combined with eccentric exercise. Eighteen successfully prepared were randomized into model, press, and press + capsaicin (TRPV1 agonist) groups (n = 6 per group). The press group received local pressing at MTrPs every two days for seven sessions, while the press + capsaicin group received intraperitoneal capsaicin prior to pressing. Pressure pain threshold (PPT) and soft tissue tension (STT), with STT quantified by the displacement at a loading force of 0.2 kg (D_0.2), were measured before and after intervention. After treatment, the MTrPs tissue and the L2-L4 dorsal root ganglia (DRG) were collected for analysis. Skeletal muscle morphology was observed by hematoxylin-eosin (HE) staining. Inflammatory mediators in MTrPs tissue were measured by enzyme-linked immunosorbent assay (ELISA). TRPV1 protein expression in DRG was detected by Western blot. Immunofluorescence was used to detect TRPV1 on CGRP⁺ fibers in MTrPs and to quantify TRPV1⁺/c-Fos⁺ cells in DRG.

Compared with the blank group, the model group showed reduced pain threshold, increased soft tissue tension, disorganized myocytes, inflammatory infiltration, elevated TRPV1 in nerve endings, increased interleukin-1β (IL-1β), prostaglandin E2 (PGE₂), calcitonin gene-related peptide (CGRP), substance P (SP), decreased interleukin-10 (IL-10), and upregulated TRPV1 and TRPV1⁺/c-Fos⁺ cells in DRG (p < 0.01 or p < 0.05). Pressing reversed these changes, restored the pain threshold, soft tissue tension, and myocyte morphology, reduced TRPV1 and pro-inflammatory mediators, increased IL-10, and downregulated TRPV1 and TRPV1⁺/c-Fos⁺ cells in DRG (p < 0.01 or p < 0.05). These effects were partially blocked by capsaicin, as the press + capsaicin group exhibited reversed effects compared with pressing alone (p < 0.01 or p < 0.05).

Pressing intervention increases the mechanical pain threshold and improves soft tissue tension in rats with MTrPs. The underlying mechanism may be associated with alleviating local inflammation, modulating the TRPV1 channel in unmyelinated C-type sensory nerve fibers, and inhibiting TRPV1 expression, thereby reducing sensory nerve excitability.