Safflor Yellow B Attenuates Ischemic Brain Injury via Downregulation of Long Noncoding AK046177 and Inhibition of MicroRNA-134 Expression in Rats

Figure 1

Effect of safflor yellow B on neurological deficit score, infarction area, total motor score, and cAMP level. (a) Chemical structure of safflor yellow B. As shown in (b)–(e), rats were divided into six groups: sham, ischemia/reperfusion (I/R), AK046177 siRNA, AK046177 siRNA+miR-134 agomir, SYB, SYB+miR-134 agomir. Except for the sham group, all rats in the other groups had established ischemia for 1 h followed by reperfusion for 23 h. SYB and saline were administrated by tail vein continuously for three days before treatment with I/R, and miR-134 agomir and AK046177 siRNA were given via intracerebroventricular injection. The neurological deficit score of each rat was obtained according to Longa’s method. Infarct volumes were measured by staining brain sections with 2,3,5-triphenyltetrazolium chloride. (a) represents pathological changes of cerebral infarction ((a) sham; (b) I/R; (c) AK046177 siRNA; (d) AK046177 siRNA+miR-134 agomir; (e) SYB; (f) SYB+miR-134 agomir). (b) represents neurological deficit scores. (c) represents the infarction area. (d) represents total motor scores (). As shown in (f)–(g), cAMP levels in the cerebral cortex and primary fetal cortical cells were detected using a ¹²⁵I-radioimmunoassay according to the method described by the manufacturer. Data are presented as ( in tissues; in cells). One-way ANOVA test was used to determine statistical significance. vs. the sham group or the control group, ^##vs. the I/R group or the OGD/R group, ^Δ or ^ΔΔvs. the AK046177 siRNA group, and ⁺ or ⁺⁺vs. the SYB group.

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