Sodium tanshinone IIA sulfonate improves inflammation, aortic endothelial cell apoptosis, disseminated intravascular coagulation and multiple organ damage in a rat heat stroke model

The aim of the present study was to investigate the effects of sodium tanshinone IIA sulfonate (STS) on inflammatory responses, aortic endothelial cell apoptosis, disseminated intravascular coagulation (DIC) and multiple organ damage in an animal model of classic heat stroke (CHS). The rats in the heat stroke (HS) and STS-treated heat stroke (STS-HS) groups were placed into a pre-warmed animal temperature controller (ATC) at 35 degrees C. The moment at which the rectal temperature reached 43.5 degrees C was considered as the time of onset of HS. In the HS groups, the rats were removed from the ATC and allowed to recover at 26 degrees C for 0, 2, 6 or 12 h. In the STS-HS groups, the rats received femoral vein injections of 5-40 mg/kg STS immediately following the onset of HS and were subsequently placed at a temperature of 26 degrees C to recover for 6 h. In the present study, the serum levels of tumor necrosis factor (TNF)-alpha, interleukin (IL)-1 beta and IL-6 were assessed using ELISA, and the numbers of apoptotic aortic endothelial cells were investigated using terminal deoxynucleotidyl transferase deoxyuridine triphosphate nick-end labeling combined with immunofluorescence. In the HS groups, the serum levels of TNF-alpha, IL-1 beta and IL-6, as well as the numbers of apoptotic aortic endothelial cells were increased compared with the normothermic control group. Additionally, the plasma prothrombin time, activated partial thromboplastin time and D-dimer level were significantly increased in the HS group compared with the normothermic control group following recovery for 6 h. By contrast, the platelet count was decreased in the HS group compared with the normothermic control group. The serum levels of creatinine, blood urea nitrogen, alanine aminotransferase, aspartate aminotransferase, alkaline phosphatase and lactate dehydrogenase were increased and histopathological damage to multiple organs was observed in the HS group following recovery for 6 h. In the STS-HS groups, cytokine levels and apoptotic aortic endothelial cell numbers were reduced compared with the HS group after 6 h recovery. STS (40 mg/kg) treatment additionally improved the serum levels of organ injury indicators and plasma indicators of coagulopathy, and prevented histopathological damage to multiple organs. These findings demonstrated that STS treatment may ameliorate multiple organ damage by attenuating inflammatory responses, aortic endothelial cell apoptosis and DIC in CHS. These results suggested that STS may hold potential as an alternative therapeutic strategy for the treatment of patients with HS.