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The role of oxidative stress in the acute liver injury of rats with heat stroke and its mechanism
Author(s): 
Pages: 285-289
Year: Issue:  4
Journal: Medical Journal of Chinese People's Liberation Army

Keyword:  heat strokeoxidative stressliver injury;
Abstract: Objective To investigate the role of oxidative stress in acute liver injury in a heat stroke model of conscious rats, and to explore its underlying mechanism. Methods Thirty-two rats were randomly(by using a random number table) assigned into a sham-heated control group(Sham group, n=8), a sham-heated group treated with NAC(Sham-NAC group, n=8), a heat stroke group(HS group, n=8) and a heat stoke group treated with NAC(HS-NAC, n=8). Rats were prepared with pre-warm chamber to initiate heat stoke. The change of rectum temperature(Tr), heart rate(HR) and systolic blood pressure(SBP) were monitored, and the time point of HS onset was recorded. Rats were sacrificed 12 h after HS onset. ALT, serum TBIL, IL-6, IL-1β, TNF-α, MDA, T-SOD and GSH in the liver homogenates were measured. Liver tissues were harvested for determining the concentration of reactive oxygen species(ROS), neutrophil infiltration and the histological changes. Results During HS onset, no significant differences were observed in Tr, HR, SBP and heat exposure time between HS group and HS-NAC group(P>0.05). However, the survival time was significantly longer in HS-NAC group than in HS group(P=0.039). 12 hours after HS onset, the concentrations of ROS and MDA in the liver homogenates were significantly higher in HS group than in the other groups(P=0.000), while the concentrations of T-SOD and GSH were much lower than in the other groups(P=0.000). The serum concentrations of ALT and TBIL were significantly higher in HS group than in the other groups(P=0.000). Compare with HS group, the pathological injury was alleviated in HS-NAC group(P=0.000). The neutrophil infiltration level and the concentrations of IL-6, IL-1β and TNF-α in liver tissue were significantly higher in HS group than in HS-NAC group(P=0.000). Conclusion Oxidative stress may play an important role in the pathogenesis of HS liver injury through its cytotoxic effect and by inducing inflammatory responses.
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