Abstract
The inflammatory process after traumatic fracture and soft tissue injury includes release of inflammatory cytokines and activated polymorph nuclear cells (PMN) that can cause subsequent affected limbs delayed healing and vital organ complications. Analgesics have good effect on relief of the symptom but may cause further burden for hepatic and renal metabolism. Freshwater clam extract (FCE) has been demonstrated to suppress the release of the pro-inflammatory cytokine tumor necrosis factor-α production after hemorrhagic shock, and decrease the level of liver injury marker in rats. The aim of the present study was to determine whether FCE is able to affect the inflammation induced by unilateral tibial fracture in a rat model. The rats were randomly divided into control, fracture, FCE and fracture with FCE groups. The fracture group received left tibia and fibula shaft fractures using a consistent three point bending method. For the fracture with FCE group, FCE (40 mg/kg) was administered orally after fracture. Their physiological changes were continuously monitored for 48 h. Blood samples were extracted from the femoral arterial catheter at 1, 3, 6, 9, 12, 18, 24 and 48 h after fracture. In comparison with fracture group, those whom were fed with FCE had more stable heart rate frequency, lower central temperature at the initial h, and lower serum level of the proinflammatory cytokines and muscle damage markers induced by fracture. FCE was also associated with decreased recruitment of inflammatory cells in the adjacent soft tissue. Thus, the present results suggest that FCE could decrease fracture induced inflammation reaction and have beneficial regulatory effect on post inflammatory response.