| Cell, as well as organisms, have several ways to defend themselves against injuries and stress. Heat shock response (HSR) , or stress response , is perhaps the oldest and most conserved form of reaction to stress . Heating cells or organisms generates the expression of a class of proteins , knows as heat shock proteins (HSP). The response and the protein structure are universal, having been found in all organisms from bacteria to humans. The HSR has important protective effects. In this work, We have studied the effects of previously induced HSP70 on deep partial thickness burn in mouse. Our objective was to test the hypothesis that heat shock response elicited before burns is protective and prevent the progressive necrosis in deep partial thickness bum, This could have a role in future clinical application of HSR induction.Methods and materialsA total of 28 KunMing mouse , weighing 35 - 38g were randomly assigned to two groups ; the control group, n = 14, the study group (heat shock/burns) , n = 14. the two groups were anesthetized with drug (30mg/kg). and the back were shaved. After one day the studygroup were anesthetized with the same anesthetic method and placed into a warm box at 44℃ for 30 minutes . after ten hours , the two groups were left into the 90℃ water for 5 seconds . Thus, the deep partial degree lesions 50% of the body surface were produced, as confirmed by histopathological studies. The all mouse would be killed and the tissues of burn wounds were excised(1 x 1cm2) at various times, while was made into segments . The segments were used to detected the changes of the tissues of burn wounds. Inmunohistochemical methods were employed to examine the contents of HSF70 . Data were analyzed statistically using t - test .Results1. The tissues of burn wounds were detected : the study and control groups were detected that the epidermis has putrefied , the dermis has degenerated and hypodermic expanded , the surviving subsidiary of skin was detected , the study group have been observed that the burn wounds has not changed at 3h in postburns , until 48 h the burn wounds of the study group has not obvious changed . However , the control group has been detected that dermal vascular occlusion was found at 6h in postburns , at 12h , the partial surviving subsidiary of skin have putrefied and at 48 h the necrosis has become more serious .2. HSP70 detection; Immunohistochemical staining clealy showed heat shock protein in the study group was determined after heating and at other serial time points . and not in the control animal in prebums. The level of HSP70 in the study group was higher than the control group all though . There was an significantly difference between the two groups (P < 0.05) .DiscussionThe heat shock response is a basic form of stress response that exists at the cellular level. Outstanding feature of the heat shock response relevant to this work are summarized by the following points; the heat shock response can be induced by several forms of stress other than heat, such as ischemia, hypoxia, hypoglycemia, and several cellular toxin; after induction of the heat shock response, the cell, tissue , or whole organism is protected against the injurious effects of the stress agent; crossprotection is observed; i. e. , the stress ?conditioned organism is also protected against other stress agents; and after the organism is stressed, there is an absolute requirement for a recovery period (6 to 8 hours) before a second stress can be tolerate. It is during this time that the organism synthesizes heat shock or other stress proteins.In this work, a heating protocol using a warm box induced HSR in a way that was sufficient to impart protection to animal submitted to burns after heating. This is a simple and inexpensive method for HSR induction. In this work, no animals died. Previously heat - shock animals had a massive expression that was significantly higher than that of untreated animals. This finding corroborates those obtained by others in other animal models. Hea...
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