Abstract: Objective To explore the effects of siRNA for epidermal growth factor receptor (EGFR) on rat brain injury after intracerebral hemorrhage and its related mechanisms. Methods The intracerebral hemorrhage model was established by injecting of VII collagenase into the caudate nucleus in rats. Rats were then treated with injection of 10 μL empty viral vector or EGFR siRNA lentivirus expression vector into lateral ventricles. The neurological function score was evaluated, and HE staining was used to observe the pathological changes of cerebral tissues. Brain water content was examined by the dried and wet weight method. EGFR expression was measured using immunohistostaining. Glial fibrillary acidic protein (GFAP) mRNA levels were analyzed through fluorescence real-time quantitative PCR. Western blot was used to detect EGFR, GFAP, signal transducers and activators of transcription 3 (STAT3) and phosphorylated STAT3 (p-STAT3). Results With the extension of intracerebral hemorrhage time, ERGF expression in cerebral tissues around hemotomas was gradually upregulated, and reached the peak on day 7 (P<0.01). In comparison with model group, EGFR siRNA relieved pathological impairment of cerebral tissues, reduced neurological function score and brain water content, and decreased the expression levels of EGFR, GFAP and p-STAT3 in cerebral tissues around hemotomas (P<0.01). Conclusions Gene silence of EGFR inhibits the activation of astrocytes through blockade of STAT3 phosphorylation, leading to reduced brain injury after intracerebral hemorrhage in rats.

Key words: intracerebral hemorrhage, EGFR, siRNA, GFAP, STAT3