Objective To investigate the preventive and therapeutic effects and the mechanisms of pyrrol idine dithiocarbamate (PDTC) on the atrophy of denervated skeletal muscle. Methods Thirty adult Wistar rats of either gender, weighing (200 ± 10) g were randomly divided into 3 groups: group A (n=6, control group), group B (n=12, denervation group), and group C (n=12, PDTC treatment group). The sciatic nerves of the rats were only exposed without cutting off in group A, and the rats were made denervated gastrocnemius models in groups B and C. PDTC of 100 mg/(kg?d) was injected peritoneally in group C and an intraperitoneal injection of the same amount normal sal ine was given in group B. After 14 and 28 days, the gastrocnemius was harvested to measure the ratio of muscle wet weight; the levels of nuclear factor of κB (NF-κB)p65 protein and the opening of the mitochondrial permeabil ity transition pore (MPTP) in the gastrocnemius were detectedrespectively by Western blot and laser confocal scanning microscope; and the apoptotic cells in atrophic muscle were measured with TUNEL. Results The ratio of muscle wet weight in group A was 1.039 ± 0.115, and it significantly decreased in groups B and C (P lt; 0.05); after 14 and 28 days of operation, the ratio of muscle wet weight in group C significantly increased when compared with those in group B (P lt; 0.05). The expression of NF-κB p65 protein in group A was 0.224 ± 0.041; the expressions of NF-κB p65 in groups B and C significantly increased when compared with that in group A (P lt; 0.05); however, the expression of NF-κB p65 in group C was significantly lower than that in group B (P lt; 0.05). The MPTP fluorescence intensity in group A was 31.582 ± 1.754; the MPTP fluorescence intensity was significantly lower in groups B and C than in group A (P lt; 0.05), and the MPTP fluorescence intensity in group C was significantly higher than that in group B (P lt; 0.05). The rate of apoptosis in group A was 4.542% ± 0.722%; after 14 and 28 days of operation, the rates of apoptosis significantly increased when compared groups B and C with group A, and signiticantly decreased when compared group C with group B (P lt; 0.05). Conclusion PDTC can retard denervated skeletal muscle atrophy, and the effect may have a relationship with its inhibition on NF-κB, the opening of the MPTP, and the ratio of apoptosis.
Objective To investigate the current status and influencing factors of decision conflict regarding disease-modifying therapy in patients with spinal muscular atrophy (SMA), aiming to provide references for future interventions to improve the quality of patient decision-making. Methods Using convenience sampling, SMA patients admitted to the Department of Neurology, West China Hospital of Sichuan University between January 2023 and October 2025 were selected as study participants. Data were collected through questionnaires assessing general demographic characteristics, the Control Preferences Scale, and the Decisional Conflict Scale (DCS). Univariate analysis and multiple linear regression were employed to explore factors influencing patients’ decisional conflict. Results A total of 70 questionnaires were distributed, with 66 valid responses returned, resulting in an effective response rate of 94.3%. The standardized DCS score of SMA patients was 35.61±21.28, indicating moderate decisional conflict. Multiple linear regression analysis revealed that age [unstandardized partial regression coefficient (b)=?0.818, 95% confidence interval (?1.383, ?0.252), P=0.005] and residential location [b=?12.660, 95% confidence interval (?19.822, ?5.498), P=0.001] were independent influencing factors for decisional conflict, collectively explaining 35.0% of the variance (adjusted R2=0.318). Conclusions SMA patients exhibit moderate levels of disease-modifying therapy-related decisional conflict, with younger age and rural residence associated with more pronounced conflict. Clinical practice should focus on individual patient characteristics while enhancing decision aids and informational support to help reduce decisional uncertainty.
Denervated muscle atrophy is a common complication in patients with nerve injury and neuromuscular diseases. Its mechanism involves multiple factors such as the regulation of neurotrophic factors, imbalance of protein synthesis and degradation, inflammatory response, oxidative stress, and changes in vascular microenvironment. As a non-invasive rehabilitation intervention, passive movement has shown important potential in delaying the atrophy of denervated muscle and promoting the recovery of neuromuscular function. Compared with active exercise, passive exercise activates neural pathways with a “bottom-up” sensory feedback pathway, which can maintain residual neural connections without increasing the nerve burden, reduce inflammation, and improve local circulation and psychological state through rhythmic mechanical stimulation. However, there are still some limitations in the relevant mechanism research, such as unclear specificity, weak clinical evidence, and lack of individualized regimen parameters. This article systematically reviews the physiological and molecular mechanisms, psychological regulation mechanisms, and clinical application status of passive movement intervention for denervated muscle atrophy, and integrates the physiological-psychological synergy pathway, aiming to provide systematic theoretical support and practical reference for the rehabilitation intervention of denervated muscle atrophy.