Objective:To explore the curative effect of rehabilitation nursing on the rat knee model of post-traumatic joint contractures.Methods:Male Wistar rats ( n=40), weighing between (180±20) g, were randomly divided into control group ( n=8) and experimental group ( n = 32) by random number table. The left knee was surgically immobilized in the experimental group which by external fixation for 4 weeks which applied the Nagai method established the model of post-traumatic joint contractures, the group also divided into four groups namely experimental control group, rehabilitation nursing intervention group, drug intervention group and exercise intervention group, 8 rats in each group and they were given different interventions. After 4 weeks interventions each rat was photographed with X-ray in order to measure the range of motion of the left knee joint range of motion (ROM), the joint muscle and synovial tissue of the animals were subjected to morphological analysis. Results:The ROM of left knee joint in experimental group (74.74±9.23) ° was lower than that of in control group (109.72±5.74) ° after 4 weeks immobilization, the difference was statistically significant ( t value was 12.237, P < 0.01), which showed that the model of joint contractures was established successfully. Compared with the experimental control group ROM (72.20±12.73) °, the difference of ROM (103.54 ±4.36)° in rehabilitation nursing intervention group and ROM (98.13 ±11.20) ° in drug intervention group were significantly higher ( t value was, P < 0.05). The results of pathological section showed that the gloss of muscle tissue in the rehabilitation nursing intervention group and the muscle fiber arrangement in the drug intervention group were close to those in the control group. Conclusion:Rehabilitation nursing intervention can not only improve ROM of joint contracture model animals, but also promote the recovery of joint muscle tissue structure.

Objective:To observe any effect of supplementing treadmill training with applications of the traditional Chinese Songchi ointment in the rehabilitation of gastrocnemius muscles atrophied through disuse.Methods:Forty-five Wistar rats were randomly divided into a normal control group ( n=8) and a model group ( n=37). The rats in the model group had their left hind limbs immobilized by the Nagai method to induce disused muscle atrophy (DMA). That group was then randomly subdivided into a model control (MC) group, a treadmill training group (the EX group), a Songchi ointment group (SC group) and a comprehensive rehabilitation group (the CR group), each of 8. The EX and SC groups were given treadmill training at 18m/min or topical application of Songchi ointment once a day, 6 days a week for 6 weeks. The CR group was given both treatments. After the 6 weeks, hematoxylin and eosin staining was used to evaluate the pathological changes in the gastrocnemius of each rat′s left hind limb. Serum levels of tumor necrosis factor α (TNF-α), interleukin-1β (IL-1β) and interleukin-10 (IL-10) were detected using enzyme-linked immunosorbent assays. PI3K, Akt and mTOR mRNA and protein were assayed using real-time quantitative PCR and western blotting. Results:The arrangement of muscle fibers in the MC group was disordered and there was a large number of infiltrated inflammatory cells. Such conditions were significantly relieved in the CR group. After the intervention the levels of inflammatory factors TNF-α and IL-1β in the CR group were, on average, significantly lower than those observed in the MC group, the EX group or the SC group, while the level of anti-inflammatory factor IL-10 was significantly higher. The average PI3K, Akt and mTOR mRNA and protein levels of group CR were significantly higher than those of the MC and EX groups.Conclusions:The traditional Chinese Songchi ointment can usefully supplement treadmill training to relieve DMA. It upregulates IL-10, activates the PI3K Akt/mTOR signaling pathway and promotes the synthesis of muscle fiber protein while down-regulating TNF-α and IL-1β and muscle fiber inflammatory response.

Objective:To observe any effect supplementing treadmill training with external application of relaxation cream on skeletal muscle cell apoptosis and IGF-1/PI3K/Akt signaling.Methods:Eight Wistar rats formed a healthy control group (the healthy group) and muscle atrophy was induced in the left hind limbs of another 32. Those 32 rats were randomly divided into a model control group (model group), a treadmill training group (treadmill group), a relaxation cream group (TCM group), and a group which received both treadmill training and the relaxation cream (combined group). After 6 weeks of the intervention, terminal deoxynucleotidyl transferase nick-end labeling (TUNEL) was used to detect any apoptosis of skeletal muscle cells. Western blotting was employed to detect the protein expression levels of insulin-like growth factor 1 (IGF-1), phosphorylated PI3K (p-PI3K), phosphorylated Akt (p-Akt), B-cell lymphomato-2 (Bcl-2) and Bcl-2 associated X protein (Bax) in the skeletal muscles.Results:The number of apoptotic cells in the skeletal muscles of the treadmill, TCM and combined groups was significantly less, on average, then in the model group. The difference in the combined group was significantly greater than in the other two groups. The expression of Bcl-2 protein in the model group was significantly lower than in the healthy group, while that of Bax protein had increased significantly. Compared with the model group, a significant increase in Bcl-2 protein expression and a significant decrease in Bax protein expression were observed in both the TCM and combined groups. Compared with the model group, the expression of IGF-1, p-PI3K and p-Akt proteins had increased significantly in both the TCM and combined groups, with significantly greater increases in the combined group, on average.Conclusion:Combining treadmill training with relaxation cream can inhibit the apoptosis of skeletal muscle cells, at least in DMA rats. The mechanism may be related to activation of the IGF-1/PI3K/Akt signaling pathway, up-regulation of Bcl-2 and down-regulation of Bax.