RESUMO
INTRODUCTION: This study aimed to investigate the effect of cognitive load on anticipatory postural adjustment (APA) latency in patients with non-specific chronic low back pain (NCLBP) and its relationship with pain-related functional changes. METHODS: A cross-sectional study was conducted from December 15, 2022 to January 25, 2023. Participants were divided into a healthy control group (n = 29) and an NCLBP group (n = 29). Each group was assigned a single task of rapid arm raising and a dual task of rapid arm raising combined with a cognitive load. The cognitive load task was conducted using visual conflict. The APA latency for bilateral trunk muscles was observed using electromyography. The duration of electromyography recording in each task cycle was 28 s. Pain related-functional changes were evaluated using Roland-Morris Disability Questionnaire (RMDQ) before all tasks. RESULTS: The APA latency for the right multifidus was significantly delayed in the NCLBP group [25.38, 95% confidence interval (CI) 13.41-37.35] than in the healthy control group (- 5.80, 95% CI - 19.28 to 7.68) during dual task (p = 0.0416). The APA latency for the right multifidus (25.38, 95% CI 13.41-37.35) and transverse abdominis/internal oblique (29.15, 95% CI 18.81-39.50) were significantly delayed compared with on the left side in the NCLBP group during dual task (- 3.03, 95% CI - 15.18-9.13, p = 0.0220; 3.69, 95% CI - 6.81 to 14.18, p = 0.0363). The latency delay of the right and left multifidus APA in the NCLBP group under the dual-task was positively correlated with RMDQ scores (r = 0.5560, p = 0.0017; r = 0.4010, p = 0.0311). CONCLUSIONS: Cognitive load could induce APA delay in the right trunk muscles and co-activation pattern changes in bilateral trunk muscle APA in patients with NCLBP. The APA onset delay in multifidus is positively related to pain-related daily dysfunction. Trial Registration ChiCTR2300068580 (retrospectively registered in February 23, 2023).
RESUMO
BACKGROUND: Human-derived mesenchymal stromal cells have been shown to improve cognitive function following experimental stroke. The activity of exosomes has been verified to be comparable to the therapeutic effects of mesenchymal stromal cells. However, the effects of exosomes derived from human umbilical cord mesenchymal stem cells (HUC-MSCs) (ExoCtrl) on post-stroke cognitive impairment (PSCI) have rarely been reported. Moreover, whether exosomes derived from C-C chemokine receptor type 2 (CCR2)-overexpressing HUC-MSCs (ExoCCR2) can enhance the therapeutic effects on PSCI and the possible underlying mechanisms have not been studied. AIM: To investigate the effects of ExoCtrl on PSCI and whether ExoCCR2 can enhance therapeutic effects on PSCI. METHODS: Transmission electron microscopy, qNano® particles analyzer, and Western blotting were employed to determine the morphology and CCR2 expression of ExoCtrl or ExoCCR2. ELISA was used to study the binding capacity of exosomes to CC chemokine ligand 2 (CCL2) in vivo. After the intravenous injection of ExoCtrl or ExoCCR2 into experimental rats, the effect of ExoCtrl and ExoCCR2 on PSCI was assessed by Morris water maze. Remyelination and oligodendrogenesis were analyzed by Western blotting and immunofluorescence microscopy. QRT-PCR and immunofluorescence microscopy were conducted to compare the microglia/macrophage polarization. The infiltration and activation of hematogenous macrophages were analyzed by Western blotting and transwell migration analysis. RESULTS: CCR2-overexpressing HUC-MSCs loaded the CCR2 receptor into their exosomes. The morphology and diameter distribution between ExoCtrl and ExoCCR2 showed no significant difference. ExoCCR2 bound significantly to CCL2 but ExoCtrl showed little CCL2 binding. Although both ExoCCR2 and ExoCtrl showed beneficial effects on PSCI, oligodendrogenesis, remyelination, and microglia/macrophage polarization, ExoCCR2 exhibited a significantly superior beneficial effect. We also found that ExoCCR2 could suppress the CCL2-induced macrophage migration and activation in vivo and in vitro, compared with ExoCtrl treated group. CONCLUSION: CCR2 over-expression enhanced the therapeutic effects of exosomes on the experimental PSCI by promoting M2 microglia/macrophage polarization, enhancing oligodendrogenesis and remyelination. These therapeutic effects are likely through suppressing the CCL2-induced hematogenous macrophage migration and activation.
