Figure 2.

Silencing of lncRNA XIST aggravates cerebral ischemia-induced brain damage in vivo

(A) Efficiency of shRNA-lncRNA XIST (si-XIST) in brain tissues of mice (n = 6). ∗∗∗p < 0.001. (B) Representative images of TTC staining from brain sections of sham or the negative control (NC) shRNA (si-Ctl) and si-XIST-treated mice at day 7 post-ischemic reperfusion. (C) Quantification of infarct volume after 7 days post-ischemic reperfusion. Results are expressed as the mean ± standard deviation and analyzed by one-way ANOVA (n = 6 mice per experimental group). Note that no infarct was seen in the control (sham) brain. Compared to the si-Ctl-treated mice, si-XIST-treated mice exhibited significantly larger infarct volumes at day 7 post-ischemic reperfusion. ∗∗p < 0.01. (D) The neurological functional performance was assessed using Modified Neurological Severity Score (mNSS) evaluation before and 2, 4, and 7 days after MCAO (n = 12 mice per experimental group). Note that si-XIST-treated mice had worse functional recovery than did si-Ctl-treated mice at days 2, 4, and 7 post-ischemic reperfusion. ∗p < 0.05, ∗∗p < 0.01, and ∗∗∗p < 0.001 versus si-Ctl-treated mice.