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Objective To investigate the protective effect of heat shock protein (HSP) 70 on the acute lung injury (ALI) of rats with heat stroke. Methods Sixty four rats were randomly (by employing a random number table) assigned into a sham-heated group (Sham group), heat stress group (HS group), and HS plus gluttamine treatment group (HS+GLN group) and HS plus quercet in treatment group (HS+QU group), 16 each. All rats were housed in a artificial climate chamber, with the rats in the sham groups exposed to a temperature of 23℃ and humidity of 55%±5%, while the rats of HS, HS+GLN and HS+QU groups to an ambient temperature of 39℃ and humidity of 65%. During heat stress or sham heating, rectal temperature (Tr), systolic blood pressure (SBP) and pulse rate (PR) were monitored to observe the difference in heat stress response among the groups. The time point at which the SBP started to drop from the peak level was taken as the point of HS onset. At the onset of HS, heat exposure was terminated, then the rats were immediately removed from the chamber, and returned to room temperature. The rats were scarified 0h and 6h after HS onset respectively. After bronchoalveolar lavage fluid (BALF) was collected, the lungs of all animals were harvested for pathological examination of lung injury. The concentrations of IL-1β, TNF-α and IL-6 in BALF and HSP70 in lung homogenate were measured by using an enzyme linked immunosorbent assay kit. Results Compared with HS and HS+QU groups, the rats in HS+GLN group required significantly greater heat load to induce HS (P |
