Objective To explore the role of salidroside in HIRI and its related mechanism. MethodsA total of 90 male SD rats were randomly divided into the sham group, the model group, the low, medium and high dose group, 18 rats in each group. The low, medium and high dose group rats were injected with 7.5, 15, 30 mg/kg salidroside solution, and the sham group and model group were injected with saline in the same volume, one time per day. After 7 days, all the rats were set up with the model of IR except the rats in Sham groups. The AST and ALT of serum, contrast between groups liver tissue by Optical microscope with HE dyeing at 4, 8, 16 h after reperfusion. Western Blot was used to detect the expression of protein of MAPK, JNK, ERK and NF-κB.ResultsFour, 8, 16 h after reperfusion, the level of ALT (540.67 ± 15.91 U/L vs.697.67 ± 5.98 U/L, 307.50 ± 12.97 U/L vs.962.50 ± 17.63 U/L, 103.33 ± 3.95 U/L vs.198.17 ± 9.73 U/L) and AST (651.17 ± 7.39 U/L vs.944.67 ± 11.38 U/L, 415.50 ± 10.97 U/L vs.1561.83 ± 15.76 U/L, 168.33 ± 5.81 U/L vs. 280.33 ± 12.35 U/L) in the high dose group were significantly lower than those in the model group. Eight and 16 hours after reperfusion, the expression of MAPK (1.28 ± 0.19 vs. 2.10 ± 0.12, 1.64 ± 0.14 vs.1.89 ± 0.14), JNK (1.80 ± 0.10 vs. 2.42 ± 0.11, 0.84 ± 0.17 vs. 3.32 ± 0.19), ERK (2.43 ± 0.10 vs.5.95 ± 0.09, 2.07 ± 0.13 vs. 6.61 ± 0.14), NF-κB (2.32 ± 0.16 vs. 3.08 ± 0.10, 2.11 ± 0.13 vs. 2.74 ± 0.17) in the high dose group were significantly lower than the model group (P<0.05).Conclusions The salidroside could reduce the liver ischemia- reperfusion injury, and its mechanisms may rugulate the MAPK/NF-κB signaling pathways.

Objective To research the effect and autophagy in hepatic ischemia-reperfusion injury based on relevant indicators of the specimens of rat liver which ischemia reperfusion model by salidroside pretreatment. Methods A total of 90 male SD rats were randomly divided into the sham group, the model group, the low, medium and high dose group, 18 rats in each group. The low, medium and high dose group rats were treated with 7.5, 15, 30 mg/kg salidroside solution by gavage, and the sham group and model group and model group were filled with saline in the same volume,one time per day. After 7 days, all the rats were set up with the model of IR except the rats in sham groups. The AST and ALT of serum, contrast between groups liver tissue by Optical microscope with HE dyeing at 4, 8, 16 h after reperfusion. Western Blot was used to detect the expression of protein of LC3 and Beclin-1. The number and morphology of autophagy in each group of liver cells were observed by electron microscopy. Results After reperfusion 4, 8, 16 h, the level of ALT (662.36 ± 5.82 U/L vs. 983.67 ± 8.96 U/L, 436.49 ± 12.93 U/L vs. 1536 ± 10.77 U/L, 168.61 ± 8.34 U/L vs. 280.42 ± 17.37 U/L) of the high dose group weresignificantly lower than the model group, and the AST (513.29 ± 11.74 U/L vs. 656.38 ± 7.67 U/L, 276.29 ± 9.21 U/L vs. 930.19 ± 15.62 U/L, 97.83 ± 4.29 U/L vs. 211.23 ± 7.87 U/L) of the high dose group were significantly lower than the model group. After reperfusion 8, 16 h, the expression of LC3-Ⅱ (1.21 ± 0.16 vs. 1.91 ± 0.12, 2.00 ± 0.14 vs. 1.09 ± 0.11) in the high dose group were significantly lower than the model group, and the results were same to Beclin1 (3.53 ± 0.19 vs. 7.15 ± 0.14, 2.65 ± 0.27 vs. 7.60 ± 0.21) (P<0.05). After reperfusion 8 h, the number of autophagosome (3.24 ± 0.62 vs.7.84 ± 0.45) in the high dose group were significantly lower than the model group (P<0.05). Conclusions The hepatic ischemia-reperfusion injury was serious, and inhibiting autophagy was one of possible mechanisms to protect liver cells by salidroside.