ABSTRACT
Knee osteoarthritis (OA) is a degenerative joint disease caused tearing and progressive wear of articular cartilage, and total knee arthroplasty (TKA) is recommended to patients with OA. The purpose of this study was to investigate the effect of proprioceptive neuromuscular facilitation (PNF) and both sides up ball (BOSU) exercises on pain, range of motion (ROM), and muscle function in patients following TKA. Ten participants who have limitation of the knee joint from TKA were divided into two groups: the continuous passive motion (CPM)+PNF exercise group (n=5) and the CPM+BOUS exercise group (n=5). Exercise rehabilitation program consisted of PNF and BOSU exercises, and both exercises were performed twice a day for 2 weeks. To examine effect of exercise rehabilitation, visual analogue scale (VAS), sit and reach flexibility, knee ROM, and Timed Up and Go test (TUG) were measured before and after exercise intervention. A two-way repeated analysis of variance was used to confirm the main effect. If there was a significant interaction effect, an independent t-test between groups or a paired t-test between times was applied. VAS, sit and reach flexibility, knee ROM and TUG did not show interaction between the PNF and BOSU exercise groups, but all measured variables showed significant differences over time. Present findings provide information that PNF and BOSU exercise rehabilitation after TKA might be an important part of ensuring successful surgical outcomes as they have a positive impact on reducing pain, increasing ROM, improving muscle strength, and enhancing daily life movements.
ABSTRACT
Sinapic acid (SA) is a phenylpropanoid compound with anti-inflammatory and neuroprotective activities. The neuroprotective effects of SA in a mouse model of amyloid ß (Aß)(1-42) protein-induced Alzheimer's disease (AD) were investigated. Mice received a bilateral injection of Aß(1-42) protein into the hippocampus to verify the efficacy of SA. Mice were treated with SA (10mg/kg/day, p.o.) for 7days beginning immediately after Aß(1-42) protein injection, and an acquisition trial of the passive avoidance task was conducted 1h after the last administration of SA. Retention trial was conducted 24h after the acquisition trial, and mice were sacrificed for immunohistochemistry immediately after the retention trial. SA rescued neuronal cell death in the hippocampal CA1 region and also attenuated the increase of iNOS expression, glial cell activations and nitrotyrosine expressions induced by Aß(1-42) protein. SA significantly attenuated memory impairment in the passive avoidance task. These results suggest that SA ameliorated Aß(1-42) protein-related pathology including neuronal cell death and cognitive dysfunction via its anti-oxidative and anti-inflammatory activities, and may be an efficacious treatment for AD.
