Research Paper Volume 13, Issue 19 pp 23004—23019

lncRNA MEG3 aggravated neuropathic pain and astrocyte overaction through mediating miR-130a-5p/CXCL12/CXCR4 axis


Figure 2. Up-regulation of MEG3 promoted NP and inflammatory response. (A) After LV-MEG3 transfection, the level of MEG3 in CCI rats was examined by RT-qPCR. (B) PWT was adopted to assess the impact of MEG3 on mechanical hyperalgesia. (C) PWL was utilized to evaluate the influence of MEG3 on thermal hyperalgesia. (D) The proportion of GFAP-positive cells in CCI rats was determined by IHC; Scale bar=50 μm. (E) TUNEL staining was applied to detect the influence of MEG3 on neuronal cell apoptosis in the L4-L6 dorsal spinal cord of CCI rats; Scale bar=50 μm. (F) Levels of TNF-α, IL-6 and IL-1β in CCI rats after up-regulating MEG3 were examined by ELISA. (G, H) The contents of TLR4, COX2, iNOS, NF-κB, CXCL12, CXCR4, and Rac1 in dorsal spinal cord tissues of CCI rats after up-regulating MEG3 were monitored by WB. Data were expressed as mean±SD. n=5. ***P<0.001 (vs. Sham group). &P<0.05, &&P<0.01, &&&P<0.001 (vs. CCI+LV-NC group).