Glucocorticoid treatment inhibits intracerebral hemorrhage‑induced inflammation by targeting the microRNA‑155/SOCS‑1 signaling pathway.
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.
Department of Forensic Medicine, Soochow University, Suzhou, Jiangsu 215123, P.R. China.
Hong-Fei
HF
Xu
Jiangsu Patent Examination Assistance Center Under State Intellectual Property Office of The People's Republic of China, Suzhou, Jiangsu 215163, P.R. China.
Xiao-Yun
XY
Fang
Department of Forensic Medicine, Soochow University, Suzhou, Jiangsu 215123, P.R. China.
Shao-Hua
SH
Zhu
Department of Forensic Medicine, Soochow University, Suzhou, Jiangsu 215123, P.R. China.
Xue-Hua
XH
Xu
Department of Forensic Medicine, Soochow University, Suzhou, Jiangsu 215123, P.R. China.
Zhi-Xiang
ZX
Zhang
Department of Forensic Medicine, Soochow University, Suzhou, Jiangsu 215123, P.R. China.
Zu-Feng
ZF
Wang
Department of Forensic Medicine, Shanghai Medical College, Fudan University, Shanghai 200032, P.R. China.
Zi-Qin
ZQ
Zhao
Department of Dermatology, The Second Affiliated Hospital of Soochow University, Suzhou, Jiangsu 215123, P.R. China.
Yu-Jie
YJ
Ding
Department of Forensic Medicine, Soochow University, Suzhou, Jiangsu 215123, P.R. China.
Lu-Yang
LY
Tao
D000818:Animals; D000893:Anti-Inflammatory Agents / Q000627:therapeutic use*; D002478:Cells, Cultured; D002543:Cerebral Hemorrhage / Q000150:complications* / Q000188:drug therapy / Q000276:immunology / Q000378:metabolism; D003907:Dexamethasone / Q000627:therapeutic use*; D005938:Glucocorticoids / Q000627:therapeutic use*; D007249:Inflammation / Q000188:drug therapy* / Q000276:immunology; D008297:Male; D008813:Mice, Inbred ICR; D035683:MicroRNAs / Q000378:metabolism*; D015398:Signal Transduction / Q000187:drug effects; D000071222:Suppressor of Cytokine Signaling 1 Protein / Q000276:immunology
D000893:Anti-Inflammatory Agents; D005938:Glucocorticoids; D035683:MicroRNAs; C532623:Mirn155 microRNA, mouse; C491590:Socs1 protein, mouse; D000071222:Suppressor of Cytokine Signaling 1 Protein; D003907:Dexamethasone