OBJECTIVE: Systemic inflammatory mediators, including the high mobility group box 1 (HMGB1) protein, play important roles in the development of various inflammatory conditions. Although anticoagulants, such as antithrombin III (AT III), inhibit inflammation resulting from various causes, their anti-inflammatory mechanism of action is not well understood. Nevertheless, as heat stroke is a severe inflammatory response disease, we hypothesized that AT III would inhibit inflammation and prevent heat stress-induced acute heat stroke. METHODS: Male Wistar rats received a bolus injection of saline or 250 U of AT III per kg of body weight into the tail vein, followed by heat stress (exposure to 42 degrees C for 30 min). Levels of cytokines (interleukin-1 beta, interleukin-6, and TNF-alpha), NOx, and HMGB1 were measured in serum and tissue at regular intervals for 6 h after the heat stress induction. RESULTS: Levels of cytokines, NOx, and HMGB1 in serum decreased over time in AT III-treated rats. AT III pretreatment also reduced NOx levels during heat stress-induced inflammation. As a result, AT III pretreatment improved survival in a rat model of heat stress-induced acute inflammation. CONCLUSIONS: Our data suggest that AT III pretreatment inhibited the secretion of cytokines, NOx, and HMGB1, and prevented heat stress-induced acute inflammation.
OBJECTIVE: Systemic inflammatory mediators, including the high mobility group box 1 (HMGB1) protein, play important roles in the development of various inflammatory conditions. Although anticoagulants, such as antithrombin III (AT III), inhibit inflammation resulting from various causes, their anti-inflammatory mechanism of action is not well understood. Nevertheless, as heat stroke is a severe inflammatory response disease, we hypothesized that AT III would inhibit inflammation and prevent heat stress-induced acute heat stroke. METHODS: Male Wistar rats received a bolus injection of saline or 250 U of AT III per kg of body weight into the tail vein, followed by heat stress (exposure to 42 degrees C for 30 min). Levels of cytokines (interleukin-1 beta, interleukin-6, and TNF-alpha), NOx, and HMGB1 were measured in serum and tissue at regular intervals for 6 h after the heat stress induction. RESULTS: Levels of cytokines, NOx, and HMGB1 in serum decreased over time in AT III-treated rats. AT III pretreatment also reduced NOx levels during heat stress-induced inflammation. As a result, AT III pretreatment improved survival in a rat model of heat stress-induced acute inflammation. CONCLUSIONS: Our data suggest that AT III pretreatment inhibited the secretion of cytokines, NOx, and HMGB1, and prevented heat stress-induced acute inflammation.
Authors: A Bouchama; F Bridey; M M Hammami; C Lacombe; E al-Shail; Y al-Ohali; F Combe; S al-Sedairy; D de Prost Journal: Thromb Haemost Date: 1996-12 Impact factor: 5.249
Authors: S A al-Mashhadani; A G Gader; S S al Harthi; D Kangav; F A Shaheen; F Bogus Journal: Blood Coagul Fibrinolysis Date: 1994-10 Impact factor: 1.276
Authors: Raúl Teruel; Irene Martínez-Martínez; José A Guerrero; Rocío González-Conejero; María E de la Morena-Barrio; Salam Salloum-Asfar; Ana B Arroyo; Sonia Águila; Nuria García-Barberá; Antonia Miñano; Vicente Vicente; Javier Corral; Constantino Martínez Journal: J Biomed Sci Date: 2013-05-16 Impact factor: 8.410