Objective: Heat therapy is one of physical therapies used most commonly in chronic osteoarthritis. The therapeutic effects of heat therapy might be attributed to induce heat shock proteins in heat-stimulated cells and tissues and therefore, to inhibit cellular damages due to inflammation. In order to investigate preliminarily the therapeutic effects of heat therapy, Hsp(heat shock protein) 70 expressions by heat stimulation were measured in cultured chondrocytes and knee joint cartilages of rabbits.
Method: Five rabbits were used in total in this study. Three rabbits were used for chodrocytes culture and two rabbits were in vivo study. Chondrocytes were cultured from knee cartilages of three rabbits and treated at 33oC, 37oC, and 42oC for 20 min. In order to clarify whether heat therapy using ultrasonification can induce Hsp 70 expression in cartilage tissues, right knees of rabbits were heat-stimulated by ultrasonification for 20 min and their left knees were untreated. After 2 hours, cultured chondrocytes and cartilages were prepared and Hsp 70 expression was also observed by Western blot analysis.
Results: Hsp 70 expression was increased 1.48 folds in 42oC treated cells compared to in 37oC treated cells. The heat-stimulated cartilages showed 1.65 fold increases in Hsp 70 expression compared to the unstimulated cartilages.
Conclusion: Hsp 70 expressions were increased by heat stimulation in cultured chondrocytes as well as in cartilage tissues.
Objective: To prove that the skin of paralysed limb of spinal injured rat is more susceptible to a thermal injury than control, and to find out that the possible relating factors for explaining the increased susceptibility of skin.
Method: Of total 69 male Sprague-Dawley rats, 50 were randomly divided into two groups, the spinal injured of which cords were transected at T10-13 level and the control. They were subdivided into 5 subgroups according to the duration of thermal injury. Infrared ray was used for thermal injury. Arterial cannulation was done in the femoral artery for blood gas analysis. Temperature was measured with a digital thermometer. Biopsy samples were stained with HE, and also immunohistochemical staining for heat shock protein 70 (HSP-70) was done.
Results: After thermal injury, the spinal injured group showed more severe tissue damage and a higher temperature elevation than the control. There was a tendency of decreased blood pH and pO2, and increased pCO2. Contrary to the control, the immunoreactivity of HSP-70 was very tiny or rarely present in the spinal injured group.
Conclusion: This study suggest that the increased susceptibility of skin to the thermal injury in spinal injured rats may be related to the vasomotor instability. And, the poor expression of HSP-70 from the skin of spinal injured rat can be a factor for the explanation of the defective cellular protective response in spinal cord injury.