Ptprj-as1 mediates inflammatory injury after intracerebral hemorrhage by activating NF-κB pathway.

OBJECTIVE: We aimed at investigating the expression of long non-coding RNA (lncRNA) Ptprj-as1 and the role of lncRNAPtprj-as1 in inflammatory cells after intracerebral hemorrhage and its potential mechanism.
MATERIALS AND METHODS: The rat model of intracerebral hemorrhage was established. Expressions of Ptprj-as1 and inflammatory cytokines in inflammatory cells were detected by quantitative Real-time PCR (qRT-PCR). After BV2 cells were transfected with lentivirus, cell proliferation, migrative ability and apoptosis were detected by cell counting kit-8 (CCK-8) assay, transwell chamber and flow cytometry, respectively. Immunofluorescence was used to explore the ratio of M1 and M2 glial cells. The detection of tumor necrosis factor alpha (TNF-α) expression was performed using enzyme-linked immunosorbent assay (ELISA). Moreover, the expressions of key genes in NF-κB pathway were evaluated using Western blot.
RESULTS: Ptprj-as1 was highly expressed in inflammatory tissues caused by intracerebral hemorrhage (ICH). Overexpressed Ptprj-as1 promoted the migration of BV2 cells and expression levels of inflammatory cytokines such as TNF-α, interleukin-1β (IL-1β), interleukin-6 (IL-6), iNOS and NO. Meanwhile, Ptprj-as1 enhanced the proportion of M1 glial cells, the mechanism of which might be related to the activation of NF-κB pathway.
CONCLUSIONS: Ptprj-as1 activates NF-κB pathway in microglia and promotes the secretion of inflammatory cytokines, which is involved in inflammatory injury caused by intracerebral hemorrhage.