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 1. Expression levels of circLrp1b, miR-27a-3p, Dram2, and autophagy-associated molecules in traumatic brain injury rats treated with dexmedetomidine. (A) circLrp1b in traumatic brain injury (TBI) brain tissues. Divergent primers detect circular RNAs in cDNA, but not in gDNA. GAPDH served as a negative control. (B) Abundance of circLrp1b and Lrp1b mRNA, as determined using quantitative real-time reverse transcriptase polymerase chain reaction (qRT-PCR), in injured brain tissues treated with or without RNase R; cDNA, complementary DNA; gDNA, genomic DNA. ***p < 0.001, compared with mock. After the rats were subjected to TBI, intraperitoneal injection of 20 μg/kg dexmedetomidine (DEX) was administered for 4 consecutive days. Expression levels of circLrp1b (C), miR-27a-3p, (D) and Dram2 (E) in Sham, Sham + DEX, TBI, and TBI + DEX groups, as determined using qRT-PCR. Each experiment was repeated 6 times. **p < 0.01, ***p < 0.001; ns, not significant, compared with Sham; #p < 0.05, ##p < 0.01, ###p < 0.001, compared with TBI. (F) Expressions of the Dram2, ATG5, Beclin-1, p62, and LC3 I/II proteins, as measured by western blot.