Minocycline inhibits nerve cell apoptosis caused by intracerebral hemorrhage in young mice via TRAIL signaling pathway

Abstract

Purpose: To investigate the influence of minocycline on nerve cell apoptosis caused by intracerebral hemorrhage (ICH) in young mouse model, and the mechanism of action involved. Methods:C57BL/6 mice were divided into control group, ICH group and minocycline treatment group (MC group, 25 mg/kg). Terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) assay was conducted to determine nerve cell apoptosis in the brain tissues. The expression levels of genes and proteins related to apoptosis and TRAIL signaling pathway were measured by reverse transcription-polymerase chain reaction (RT-PCR) and Western blotting.Results: The levels of Glu, Cr, Na+, IL-6, IL-1β and TNF-β were significantly increased in ICH group, and the content of K+ was significantly raised in MC group (p < 0.05). TUNEL staining showed that there were more apoptotic cells, dominated by glial cells in ICH group, and fewer apoptotic cells in MC group. Gene assay results indicate that ICH group exhibited markedly raised mRNA levels of caspase-3, TNF-β and TRAIL1, as well as lowered levels of B-cell lymphoma-2 (Bcl-2) (p < 0.05). The results of protein assay showed that the protein levels of caspase-3 and TRAIL1 rose while that of Bcl-2 declined significantly in ICH group. However, the expression trends of the genes and proteins in MC group were the opposite of those in the ICH group.Conclusion: Minocycline inhibits nerve cell apoptosis caused by ICH in the young mouse model by repressing the expression of the TRAIL signaling pathway. The findings may provide new insight intothe treatment of ICH.