Modulation effects of pressing manipulation on local inflammatory responses and ERK/NF-κB pathway in trigger point model rats

To investigate the mechanism of trigger point deactivation induced by pressing manipulation in a rat model and to explore its potential regulation of the inflammatory response through the extracellular signal-regulated kinase (ERK)/nuclear factor-κB (NF-κB) pathway.

Fifty male Sprague-Dawley rats were randomly divided into a blank group, a model group, a pressing manipulation group, an ERK agonist group, and a pressing manipulation + ERK agonist group, with 10 rats in each group. Except for the blank group, rats in other groups were used to establish the trigger point rat model using the blunt blow combined with the eccentric exercise method. The pressing manipulation group underwent pressing manipulation treatment at the trigger points. The ERK agonist group received an injection of recombinant human epidermal growth factor via the tail vein. The pressing manipulation + ERK agonist group received interventions from both the pressing manipulation and ERK agonist groups. The pressure pain threshold (PPT) was measured by a mechanical pain threshold detector before and after the intervention. The histological changes were evaluated by hematoxylin-eosin staining after the intervention; the expression levels of ERK, phosphorylated ERK (p-ERK), NF-κB p65 (p65), phosphorylated NF-κB p65 (p-p65), and phosphorylated NF-κB inhibitor (p-IκB) were detected by immunoblotting; the levels of interleukin (IL)-1β, IL-6, and tumor necrosis factor (TNF)-α were detected by enzyme-linked immunosorbent assay.

The PPT increased (P<0.05); the inflammatory cells disappeared; the ratios of p-ERK/ERK, p-p65/p65, and p-IκB/β-actin, also the levels of IL-1β, IL-6, and TNF-α all decreased in the pressing manipulation group after the intervention compared with the model group (P<0.05). The PPT decreased significantly (P<0.05), the inflammatory cell presence increased, and the ratios of p-ERK/ERK and p-p65/p65 were elevated (P<0.05); additionally, the levels of IL-6 and TNF-α were significantly higher in the pressing manipulation + ERK agonist group compared with the pressing manipulation group (P<0.05). The PPT was significantly lower (P<0.05), the inflammatory cell count was higher, the ratios of p-ERK/ERK and p-IκB/β-actin and the levels of IL-1β and TNF-α were significantly higher in the ERK agonist group compared with the pressing manipulation + ERK agonist group (P<0.05).

Pressing manipulation can effectively alleviate inflammation and pain in trigger point model rats, potentially by inhibiting the ERK/NF-κB signaling pathway.