Glucocorticoid treatment inhibits intracerebral hemorrhage‑induced inflammation by targeting the microRNA‑155/SOCS‑1 signaling pathway.

Abstract

Intracerebral hemorrhage (ICH) results in inflammation, and glucocorticoids have been proven to be effective inhibitors of ICH‑induced inflammation. However, the precise underlying mechanisms of ICH‑induced inflammation and glucocorticoid function remain largely undefined. Using a mouse ICH model, the present study demonstrated that the short non‑coding RNA molecule microRNA‑155 (miR‑155) is involved in the inflammatory process initiated by ICH in mice. Increased mRNA expression levels of miR‑155, as well as the pro‑inflammatory cytokines interferon‑β (IFN‑β), tumor necrosis factor‑α (TNF‑α) and interleukin‑6 (IL‑6), were observed in vivo following ICH. By contrast, the expression level of suppressor of cytokine signaling 1 (SOCS‑1) protein was reduced in the ICH group compared with control mice. Similar results were observed in vitro using astrocytes, the primary effector cells in ICH. Compared with wild type astrocytes, astrocytes overexpressing miR‑155 exhibited significant inhibition of SOCS‑1 protein expression levels. These results suggest that miR‑155 contributes to the development of ICH‑induced inflammation in mice by downregulating SOCS‑1 protein expression levels and promoting pro‑inflammatory cytokine (IFN‑β, TNF‑α and IL‑6) production. Expression levels of miR‑155 and pro‑inflammatory cytokines in the ICH group were significantly decreased following dexamethasone administration. This suggests that glucocorticoids attenuate ICH‑induced inflammation by targeting the miR‑155/SOCS‑1 signaling pathway in mice. In conclusion, the results of the present study demonstrated that the miR‑155/SOCS‑1 signaling pathway is required for ICH‑induced inflammation, and glucocorticoids inhibit this process by targeting the miR‑155/SOCS‑1 signaling pathway.