Inhibition of TREM1 reduces inflammation and oxidative stress after spinal cord injury (SCI) associated with HO-1 expressions

Publication date: January 2019Source: Biomedicine & Pharmacotherapy, Volume 109Author(s): Zhenhuan Li, Furong Wu, Dafeng Xu, Zhongzheng Zhi, Guanghui XuAbstractSpinal cord injury (SCI) is a devastating event, leading to the progression of chronic neuropathic pain syndrome. Triggering receptor expressed on myeloid cells 1 (TREM1) is an innate immune receptor expressed on neutrophils and monocytes/macrophages. TREM1 enhances inflammatory response in various models of diseases, but its significance in SCI remains unclear. In the present study, we attempted to explore the effects of TREM1 on the regulation of SCI. Spinal cord contusion injury was performed in wild type (WT) and TREM1-knockout (TREM1KO) mice, and real time-quantitative PCR (RT-qPCR), western blot, and immunofluorescent (IF) staining were used to calculate TREM1, inflammation and oxidative stress in spinal cord tissues 42 days after SPII. In vitro, astrocytes (AST) and BV2 cells were transfected TREM siRNA or the negative control (NC) siRNA to knockdown (KD) TREM1 expressions, followed by lipopolysaccharide (LPS) stimulation to verify the role od TREM1 in modulating SPI. The results suggested that TREM1 was highly expressed in the spinal cord tissues of WT mice after SCI. TREMKO mice exhibited improved locomotor function, mechanical and thermal hypersensitivity in the hindpaws after SCI. In addition, peripheral nerve injury-related biomarkers were down-regulated by TREM1KO in SCI mice. TREM1KO increased NeuN-staine...
Source: Biomedicine and Pharmacotherapy - Category: Drugs & Pharmacology Source Type: research