Research Paper Volume 12, Issue 21 pp 21687—21705
Dexmedetomidine inhibits inflammatory response and autophagy through the circLrp1b/miR-27a-3p/Dram2 pathway in a rat model of traumatic brain injury
Figure 6. Restoration of Dram2 abolishes 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 Dram2 before traumatic brain injury (TBI) induction, followed by intraperitoneal injection of 20 μg/kg dexmedetomidine (DEX). The expression levels of circLrp1b (A), miR-27a-3p (B), and Dram2 (C), as determined using real-time quantitative reverse transcriptase polymerase chain reaction. (D) The expression levels of Dram2, ATG5, Beclin-1, p62, LC3 I/II, caspase-1, and NLRP3 proteins, as evaluated using 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 + vector; &p < 0.05, &&p < 0.01, &&&p < 0.001, compared with sh-circLrp1b + Dram2.