Figure 4. Inhibition of miR-27a-3p reverses the effects of circLrp1b knockdown in traumatic brain injury-induced autophagy and inflammation. Rats were administered intracerebroventricular injection of lentivirus vectors of sh-circLrp1b and miR-27a-3p inhibitor before traumatic brain injury (TBI) induction, followed by intraperitoneal injection of 20 μg/kg dexmedetomidine (DEX). Expression levels of circLrp1b (A), miR-27a-3p (B), and Dram2 (C), as determined using real-time quantitative reverse transcriptase polymerase chain reaction. (D) Expression levels of the proteins Dram2, ATG5, Beclin-1, p62, LC3 I/II, caspase-1, and NLRP3, as measured by western blot. Quantitative analysis of TNF-α (E), IL-6 (F), and IL-1β (G) production in the hippocampal tissues by using enzyme-linked immunosorbent assay (ELISA). Each experiment was repeated 6 times. **p < 0.01, ***p < 0.001, compared with NC; #p < 0.05, ##p < 0.01, compared with sh-circLrp1b + miR-NC; &p < 0.05, &&p < 0.01, compared with sh-circLrp1b + inhibitor.