| First Author | Yuan K | Year | 2016 |
| Journal | Int Immunopharmacol | Volume | 40 |
| Pages | 339-346 | PubMed ID | 27673475 |
| Mgi Jnum | J:331340 | Mgi Id | MGI:6869399 |
| Doi | 10.1016/j.intimp.2016.09.011 | Citation | Yuan K, et al. (2016) Fine-tuning the expression of microRNA-155 controls acetaminophen-induced liver inflammation. Int Immunopharmacol 40:339-346 |
| abstractText | Treatment of acetaminophen (APAP) in overdose can cause a potentially serious and fatal liver injury. MicroRNA-155 (miR-155), a multifunctional microRNA, is known to mediate inflammatory responses via regulating various target genes. In this study, we aimed to study the role of miR-155 in APAP-induced liver injury, using miR-155-/- mice and miR-155 in vivo intervention. We noted that miR-155 expression was significantly increased in liver and blood after APAP treatment. Knockout of miR-155 deteriorated APAP-induced liver damage, with the elevated serum levels of AST and ALT. The levels of various inflammatory mediators, such as TNF-alpha and IL-6, were markedly augmented in livers in the absence of miR-155. Moreover, miR-155 deficiency aberrantly activated NF-kappa-B signaling via enhancing p65 and IKKepsilon expression. Finally, in vivo administration of miR-155 agomir attenuated APAP-induced liver damage, reduced the serum levels of AST and ALT, and dampened the NF-kB signaling. In conclusion, our data demonstrated that miR-155 protects the mice against APAP-induced liver damage via mediating NF-KB signaling pathway, suggesting that miR-155 might be a potential pharmaceutic target for treatment of APAP-induced liver inflammation. |
