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"Heat shock protein"

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"Heat shock protein"

Original Articles
The Effect of Steroid on Heat Shock Protein 70 Expression in mdx Mice.
Lim, Jeong Hoon , Bang, Moon Suk
J Korean Acad Rehabil Med 2009;33(1):1-4.
Objective
To investigate the effect of steroid administration on the apoptosis and heat shock protein 70 (HSP70) expression after exercise in the animal model of Duchenne muscular dystrophy. Method: We measured Bcl-2, BAX and HSP70 expression by western blotting. 20 control and 20 mdx mice were divided into free-living (n=10) and exercise (n=10) groups. Free-living and exercise groups were further divided into steroid-treated and sham-treated groups to evaluate the effect of steroid administration. Results: Apoptosis was most prominent in the sham-treated exercise group, while apoptosis was significantly reduced in the steroid-treated exercise group. HSP70 expression was maximized in sham-treated exercise group, whereas steroid administration inhibited HSP70 expression after exercise in muscular dystrophy animal model. Exercise loading was found to cause severe apoptosis but steroid administration alleviated apoptotic damage in mdx mice. sConclusion: HSP70 expression was suppressed in the steroid-treated exercise group, which suggests steroid might have major preventive effect in exercise-induced apoptosis of muscular dystrophy animal model. (J Korean Acad Rehab Med 2009; 33: 1-4)
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Expression of Heat Shock Protein 70 by Heat Stimulation in Rabbit Chondrocytes and Articular Cartilages.
Lee, Kang Hee , Ahn, Sang Ho , Jang, Seong Ho , Baek, Suk Hwan
J Korean Acad Rehabil Med 2001;25(6):1074-1080.

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.

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Skin Tissue Changes Following Thermal Injury in the Paralysed Lower Limb of Spinal Injured Rats.
Kim, Mi Jung , Sung, In Young , Han, Seung Hoon , Kong, Goo
J Korean Acad Rehabil Med 1999;23(6):1083-1094.

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.

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