Protective effects of glucocorticoid on liver injury in a rat sepsis model.

Sepsis is one of the leading causes of death with unsatisfactory current treatments. The present study assessed the liver protective effect of glucocorticoids on different levels of inflammation in septic shock rats. A rat septic shock model was established by lipopolysaccharide (LPS) injection. Rats were divided into control (Control), high-inflammation treated with hydrocortisone (HT), high-inflammation non-treatment (HNT), low-inflammation treated with hydrocortisone (LT) and low-inflammation non-treatment (LNT) groups according to the levels of serum C-reactive protein (CRP), interleukin (IL)-6 and interferon (IFN)-γ. The mean arterial pressure and heart rate changes were continuously monitored and aspartate aminotransferase (AST) and alanine aminotransferase (ALT) levels were measured by an automatic biochemical analyzer. Hematoxylin and eosin (H&E) staining was performed to observe the pathological changes of liver tissue. Western blot analysis was used to detect the expression of p38 mitogen-activated protein kinase (MAPK) and NF-κB protein. The results demonstrated that following 7 days of treatment, there were no obvious differences in the serum CRP, IL-6 and IFN-γ levels between the HT group and the control group, whilst the HNT group, LT group and LNT group were significantly different compared with the HT and control groups. H&E staining demonstrated that the liver cells in the HT group were homogeneous following 7 days of treatment. Western blot analysis determined that the phosphorylation levels of p38MAPK and NF-κB in HT group were reduced significantly compared with the LT group, while there was no obvious difference with the control group after 7 days treatment. The present results indicated that glucocorticoids have better therapeutic effect on septic shock rats with high-inflammation compared with low-inflammation rats. The present study provides a novel approach for glucocorticoid treatment of septic shock.