OBJECTIVE: To evaluate the effects of Xuebijing (XBJ) injection in heat stroke (HS) rats and to investigate the mechanisms underlying these effects. METHODS: Sixty anesthetized rats were randomized into three groups and intravenously injected twice daily for 3 days with 4 mL XBJ (XBJ group) or phosphate buffered saine (HS and Sham groups) per kg body weight. HS was initiated in the HS and XBJ groups by placing rats in a simulated climate chamber (ambient temperature 400C, humidity 60% ). Rectal temperature, aterial pressure, and heart rate were monitored and recorded. Time to HS onset and survival were determined, and serum concentrations of tumor necrosis factor (TNF)-alpha interleukin (IL)-1beta, IL-6, alanine-aminotransferase (ALT), and aspartate-aminotransferase (AST) were measured. Hepatic tissue was harvested for pathological examination and electron microscopic examination. Kupffer cells (KCs) were separated from liver at HS initiation, and the concentrations of secreted TNF-a, IL-beta and IL-6 were measured. RESULTS: Time to HS onset and survival were significantly longer in the XBJ than in the HS group. Moreover, the concentrations of TNF-alpha, IL-1beta, IL-6, ALT and AST were lower and liver injury was milder in the XBJ than in the HS group. Heat-stress induced structural changes in KCs and hepatic cells were more severe in the HS than in the XBJ group and the concentrations of TNF-alpha, IL-beta and IL-6 secreted by KCs were lower in the XBJ than in the HS group. CONCLUSION: XBJ can alleviate HS-induced systemic inflammatory response syndrome and liver injury in rats, and improve outcomes. These protective effects may be due to the ability of XBJ to inhibit cytokine secretion by KCs.
OBJECTIVE: To evaluate the effects of Xuebijing (XBJ) injection in heat stroke (HS) rats and to investigate the mechanisms underlying these effects. METHODS: Sixty anesthetized rats were randomized into three groups and intravenously injected twice daily for 3 days with 4 mL XBJ (XBJ group) or phosphate buffered saine (HS and Sham groups) per kg body weight. HS was initiated in the HS and XBJ groups by placing rats in a simulated climate chamber (ambient temperature 400C, humidity 60% ). Rectal temperature, aterial pressure, and heart rate were monitored and recorded. Time to HS onset and survival were determined, and serum concentrations of tumor necrosis factor (TNF)-alpha interleukin (IL)-1beta, IL-6, alanine-aminotransferase (ALT), and aspartate-aminotransferase (AST) were measured. Hepatic tissue was harvested for pathological examination and electron microscopic examination. Kupffer cells (KCs) were separated from liver at HS initiation, and the concentrations of secreted TNF-a, IL-beta and IL-6 were measured. RESULTS: Time to HS onset and survival were significantly longer in the XBJ than in the HS group. Moreover, the concentrations of TNF-alpha, IL-1beta, IL-6, ALT and AST were lower and liver injury was milder in the XBJ than in the HS group. Heat-stress induced structural changes in KCs and hepatic cells were more severe in the HS than in the XBJ group and the concentrations of TNF-alpha, IL-beta and IL-6 secreted by KCs were lower in the XBJ than in the HS group. CONCLUSION: XBJ can alleviate HS-induced systemic inflammatory response syndrome and liver injury in rats, and improve outcomes. These protective effects may be due to the ability of XBJ to inhibit cytokine secretion by KCs.