Objective: This study investigated the efficacy of extracorporeal shock wave therapy as well as the optimal intervention timing for extracorporeal shock wave therapy for patients with spasticity after stroke. Design: A search of randomized controlled trials was conducted in different electronic databases. We performed a meta-analysis to measure the effect of extracorporeal shock wave therapy versus sham interventions on spasticity and limb functionality. The meta-regression analysis was performed to determine the adequate intervention timing of extracorporeal shock wave therapy. The follow-up period of the outcomes was divided into the short (2 wks and ≤4 wks), and long (>4 wks and ≤3 mos) terms. Results: Thirteen studies with 677 participants were evaluated. Spasticity significantly improved throughout the follow-up duration. Limb functionality significantly improved in the short-term follow-up period. The meta-regression analysis showed that patients with stroke duration less than 45 mos may be benefited from extracorporeal shock wave therapy in improving limb function in all follow-up periods. Conclusions: Extracorporeal shock wave therapy is an effective method for reducing spasticity in patients with stroke, and the effect could be maintained for up to 3 mos. Its effects on limb functionality could persist for at least 2 wks. Patients who had stroke for less than 45 mos may have significant benefit from extracorporeal shock wave therapy in all follow-up periods.

Lidocaine injection is a common treatment for tendon injuries. However, the evidence suggests that lidocaine is toxic to tendon cells. This study investigated the effects of lidocaine on cultured tendon cells, focusing on the molecular mechanisms underlying cell proliferation and extracellular matrix (ECM) production. Tendon cells cultured from rat Achilles tendons were treated with 0.5, 1.0, or 1.5 mg/mL lidocaine for 24 h. Cell proliferation was evaluated by Cell Counting Kit 8 (CCK-8) assay and bromodeoxyuridine (BrdU) assay. Cell apoptosis was assessed by Annexin V and propidium iodide (PI) stain. Cell cycle progression and cell mitosis were assessed through flow cytometry and immunofluorescence staining, respectively. The expression of cyclin E, cyclin A, cyclin-dependent kinase 2 (CDK2), p21, p27, p53, matrix metalloproteinases-2 (MMP-2), matrix metalloproteinases-9 (MMP-9), type I collagen, and type III collagen were examined through Western blotting, and the enzymatic activity of MMP-9 was determined through gelatin zymography. Lidocaine reduced cell proliferation and reduced G1/S transition and cell mitosis. Lidocaine did not have a significant negative effect on cell apoptosis. Lidocaine significantly inhibited cyclin A and CDK2 expression but promoted p21, p27, and p53 expression. Furthermore, the expression of MMP-2 and MMP-9 increased, whereas that of type I and type III collagen decreased. Lidocaine also increased the enzymatic activity of MMP-9. Our findings support the premise that lidocaine inhibits tendon cell proliferation by changing the expression of cell-cycle-related proteins and reduces ECM production by altering levels of MMPs and collagens.

Statins are the most effective therapeutic agents for reducing cholesterol synthesis. Given their widespread use, many adverse effects from statins have been reported; of these, musculoskeletal complications occurred in 15% of patients after receiving statins for 6 months, and simvastatin was the most commonly administered statin among these cases. This study investigated the negative effects of simvastatin on skeletal muscle cells. We performed RNA sequencing analysis to determine gene expression in simvastatin-treated cells. Cell proliferation and migration were examined through cell cycle analysis and the transwell filter migration assay, respectively. Cytoskeleton rearrangement was examined through F-actin and tubulin staining. Western blot analysis was performed to determine the expression of cell cycle-regulated and cytoskeleton-related proteins. Transfection of small interfering RNAs (siRNAs) was performed to validate the role of cofilin and stathmin in the simvastatin-mediated inhibition of cell migration. The results revealed that simvastatin inhibited the proliferation and migration of skeletal muscle cells and affected the rearrangement of F-actin and tubulin. Simvastatin reduced the expression of cofilin and stathmin. The knockdown of both cofilin and stathmin by specific siRNA synergistically impaired cell migration. In conclusion, our results indicated that simvastatin inhibited skeletal muscle cell migration by reducing the expressions of cofilin and stathmin.

Skeletal muscle injuries are prevalent in competitive sports, often disrupting elite athletes' training programs. Platelet-rich plasma (PRP) is abundant in growth factors, cytokines, and chemokines, making it a potential solution for treating muscle injuries. Adipose-derived stem cells (ADSCs) therapy presents promise for tissue regeneration, given their self-renew and differentiation capabilities. This study aims to investigate the impact of PRP on ADSCs, with a focus on cell migration. ADSCs were isolated from the subcutaneous adipose tissue of Sprague Dawley rats. Subsequently, these ADSCs were treated with PRP. The migration ability was assessed through in vitro wound assays, migration assays, and cell spreading assays. Molecular analysis, employing Western blot, was performed to examine the expression levels of phosphorylated focal adhesion kinase (FAK), FAK, phosphorylated paxillin, paxillin, and vinculin. The filamentous actin (F-actin) cytoskeleton formation was assessed through immunofluorescence staining. The study revealed a positive impact of PRP on ADSC migration in the in vitro wound assay, migration assay, and cell spreading assay. PRP elevated the expression levels of phosphorylated FAK, FAK, phosphorylated paxillin, paxillin, and vinculin in ADSCs. Additionally, PRP affected the distribution of F-actin in ADSCs. Furthermore, siRNA-mediated knockdown of FAK and paxillin confirmed their essential roles in PRP-enhanced ADSC migration. In conclusion, our findings demonstrated that PRP promoted the migration, spreading, in vitro wound healing, and cytoskeleton rearrangement of ADSCs by upregulating the expressions of phosphorylated FAK, FAK, phosphorylated paxillin, paxillin, and vinculin. This insight supports the potential use of PRP in combination with ADSCs for regeneration therapies.