Inhibition of microRNA-155 relieves sepsis-induced liver injury through inactivating the JAK/STAT pathway

The present study aimed to investigate whether the microRNA (miR)-155 inhibitor has an anti-inflammatory effect on sepsis-associated liver injury and whether this effect is associated with the activity of the janus kinase (JAK)/signal transducer and activator of transcription (STAT) pathway. BALB/c mice were randomly divided into three groups (n=40 per group): Control, lipopolysaccharide (LPS) and miR-155 inhibitor plus LPS groups. Liver injury was induced by injection of LPS (20 mg kg(-1)). In the inhibitor plus LPS group, LPS was administered after injecting the miR-155 inhibitor (80 mg kg-1) for 3 days. Liver tissues were collected at 6, 12, 24 and 48 h after LPS exposure. Hematoxylin and eosin was used to identify the histological changes in the liver. The expression levels of miR-155, suppressor of cytokine signaling 1 (SOCS1) and STAT1 were determined by reverse transcription-quantitative polymerase chain reaction. The protein expression of tumor necrosis factor (TNF)-alpha and interleukin (IL)-10 were detected by ELISA. miR-155 inhibitor pretreatment alleviated the symptoms of LPS-exposed mice, and reduced LPS-induced mortality and liver injury. Compared with the LPS group, expression of miR-155 was significantly reduced in the miR-155 inhibitor plus LPS group at 6 h (P<0.05). SOCS1 expression was significantly increased in miR-155 inhibitor plus LPS group compared with the control and the LPS group at 12 h (P<0.05). There was a lower level of STAT1 in the miR-155 inhibitor plus LPS group compared with the LPS group (P<0.05). In addition, TNF-alpha and IL-10 were significantly decreased in the miR-155 inhibitor plus LPS group compared with the LPS group (P<0.05). In conclusion, the miR-155 inhibitor relieves liver injury by enhancing the expression of SOCS1 and inactivating JAK/STAT signaling.