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Background. Studies have found that microRNA (miR) is abnormally expressed in intracerebral hemorrhage (ICH) and is considered a therapeutic target for ICH. Objective. To investigate the expression and role of miR-126 in the ICH rat model. Methods. The ICH rat model was established, and miR-126 agomir and ZEB1 antagomir were injected into the lateral ventricle of ICH rats. The neurological function and water content of brain tissue were evaluated 48 hours later. Brain tissue around the hematoma of rats was taken to detect the expression of miR-126, ZEB1, glial fibrillary acidic protein (GFAP), and inflammatory cytokines (TNF-α, IL-1β, and IL-6). The luciferase reporter gene was applied to analyze the relationship between miR-126 and ZEB1. Results. miR-126 was downregulated in the ICH rat model, while ZEB1 was upregulated. miR-126 agomir or ZEB1 antagomir injection could improve neurological function and cerebral edema in ICH rats. In addition, it could also reduce the expression of TNF-α, IL-1β, IL-6, and GFAP in the brain tissue of ICH rats. Luciferase reporter gene showed that ZEB1 could be targeted and regulated by miR-126. Conclusion. miR-126 is downregulated in ICH rats, and miR-126 can reduce brain injury in ICH rats by inhibiting ZEB1 expression.

Increasing miR-126 Can Prevent Brain Injury after Intracerebral Hemorrhage in Rats by Regulating ZEB1