Objective Intracerebral hemorrhage (ICH) is a common cerebrovascular disease with high mortality and poor prognosis. Therefore, the biological function and underlying molecular mechanism of miR-26a in inflammatory injury following ICH was investigated. Methods The potential role of miR-26a was investigated in lipopolysaccharide (LPS)-treated microglial cells by quantitative real-time PCR. To explore the potential role of HMGA2 in the miR-26a-regulated inflammatory response, LPS-induced microglial cells were cotransfected with an miR-26a mimic and pcDNA-HMGA2. Then, lentivirus-mediated overexpression of an miR-26a mimic in mouse microglial cells was performed, and the effects of miR-26a treatment on IL-6, IL-1β, and TNF-α expression in the mouse brain, neurological behavior, and rotarod test performance of mice after ICH were observed. Results MiR-26a was significantly downregulated in LPS-treated microglia and ICH mouse models. MiR-26a markedly reduced IL-6, IL-1β, and TNF-α expression in LPS-treated microglial cells. Furthermore, HMGA2 was verified as a direct target of miR-26a. In vivo, miR-26a overexpression in mouse microglial cells significantly suppressed proinflammatory cytokine expression in mouse brains and markedly improved the neurological behavior and rotarod test performance of mice after ICH. Conclusion MiR-26a remarkably inhibited proinflammatory cytokine release by targeting HMGA2, indicating that miR-26a could protect against secondary brain injury following ICH.

Background This study aimed to evaluate the predictive value of long non‐coding RNA (lncRNA) antisense non‐coding RNA in the INK4 locus (ANRIL) for atrial fibrillation (AF) patients with ischemic stroke and investigate its correlation with risk factors, functional outcome, and prognosis. Methods A total of 386 consecutive AF patients were recruited. AF patients were followed up for 24‐48 months by outpatient follow‐up, telephone follow‐up, and medical record. The time of ischemic stroke in patients with AF was recorded, and follow‐up was continued for 6 months. LncRNA ANRIL expression from serum was detected by quantitative real‐time polymerase chain reaction (qRT‐PCR). Results Compared with the AF with ischemic stroke group (14.3 ± 2.3), patients in the AF without ischemic stroke group (11.9 ± 1.8) had significantly lower serum lncRNA ANRIL levels ( P < .05). The sensitivity and specificity of lncRNA ANRIL for identifying AF with ischemic stroke were 76.6% and 81.4%, respectively. Spearman correlation analysis results shown that lncRNA ANRIL was significantly correlated with the NIHSS score ( r Spearman = .490, P < .001) and the mRS score ( r Spearman = .466, P < .001). Compared with the lncRNA ANRIL high‐expression group, the recurrence‐free survival (RFS) of the lncRNA ANRIL low‐expression group was significantly higher ( χ 2 = 11.009, log‐rank P < .001). Cox proportional regression model analysis indicated that the serum lncRNA ANRIL level ( P = .004), NIHSS score ( P = .001), infarct volume ( P = .035), and smoking ( P < .001) were the risk factors for AF with ischemic stroke. Conclusion Serum lncRNA ANRIL exerts a good predictive value for AF with ischemic stroke, and its increased expression is correlated with worse RFS for patients.

No abstract