Objective    To study the protective mechanism of S-adenosylmethionine (SAM) underlying liver injury induced by lipopolysaccharides (LPS).     Methods    One hundred BABL/c mice were randomly divided into LPS group and SAM group. Mice in LPS group were intraperitoneally injected with 10 mg/kg LPS

and the mice in SAM group were injected with 100 mg/kg SAM 2 h before receiving the same dose of LPS. The survival rate of mice in 2 groups was recorded in 24

48

72 and 120 h after LPS injection. Histopathological changes in liver of mice were examined in 0

1

3

6

12 and 24 h after LPS injection. Tumor necrosis factor-α (TNF-α) and interleukin-10 (IL-10) levels in serum were measured by ELISA analysis at above time points. Expression of Toll-like receptor 4 (TLR4) and liver X receptor α (LXRα) in hepatic tissues was detected by immunohistochemistry and Western blotting.     Results    SAM increased the survival rate of mice from 50.0%

40.0%

30.0%

and 30.0% before LPS injection to 80.0%

70.0%

60.0%

and 50.0% after its injection (P0.05)

and attenuated the LPSinduced pathologic changes in liver tissue. The serum TNF-α level was significantly lower in SAM group than in LPS group (718.83±53.27  vs 1791.79±122.19 pg/ml

P0.05)

while the serum IL-10 level was significantly higher in SAM group than in LPS group (418.69±38.77  vs 347.09±31.37 pg/ml

P0.05) with its peaking shifted to the left. The expression level of LXRα in hepatic tissue was significantly higher while that of TLR4 in hepatic tissue was significantly lower in SAM group than in LPS group (gray value of Western blotting for TLR4：1.550±0.034 vs 1.365±0.017

for LXRα：1.605±0.027 vs 1.375±0.014

P0.05).     Conclusion    SAM can significantly attenuate LPS-induced liver injury by reducing the expression of TLR4 and increasing the expression of LXRα in liver cells

and thus lead to TNF-α decreased and IL-10 increased.