Heat stroke (HS) has been shown to induce intestinal barrier dysfunction during whole body hyperthermia. HS-induced intestinal permeability change may result from modulation of aquaporin (AQP) expression, which subsequently regulates water homeostasis. This study aimed to evaluate AQP expression in the intestine of rats with HS at different recovery time points. Sprague-Dawley (SD) rats were exposed to an ambient temperature of 40 ± 0.5°C until a maximum core temperature of 40.5°C was attained. The small intestine was surgically removed and histologically examined, and AQP expression was determined by reverse transcription polymerase chain reaction and immunohistochemical staining. H&E staining revealed those intestinal villi were destroyed from HS0 to HS1 and rebuilt from HS3 to HS12. We further stain with activated caspase 3 found expressed at HS0 and back to normal at HS3. Investigation of AQP mRNA expression identified 10 genes. PCR results of AQP1, 3, 7, 8, and 11 transcripts were significantly higher in the HS group than in the sham group. Immunohistochemical staining showed a more than 11-fold increase in AQP3 and 11 expressions at HS0. AQP1 and 8 increased at HS1 and AQP7 increased at HS3 compared with those in the sham group. In this study, we found HS induced jejunum damage and cell apoptosis. AQPs were upregulation/downregulation after HS in different time point suggested that water/glycerol transport was important when hyperthermia occurred. Furthermore, the biological function of the AQP needs more exploration in response to HS.
|Number of pages||12|
|Journal||International Journal of Clinical and Experimental Pathology|
|Publication status||Published - 2015|
- Journal Article
- Research Support, Non-U.S. Gov't