Research Paper Volume 13, Issue 6 pp 8127—8145
Long noncoding RNA NKILA transferred by astrocyte-derived extracellular vesicles protects against neuronal injury by upregulating NLRX1 through binding to mir-195 in traumatic brain injury
Figure 5. NKILA promotes proliferation and inhibits apoptosis of injured neurons by increasing NLRX1 expression via miR-195. The injured neurons were introduced with oe-NKILA + sh-NC, oe-NKILA + sh-NLRX1, miR-195 inhibitor + sh-NC, miR-195 inhibitor + sh-NLRX1, sh-NLRX1 or sh-NC. (A) cell proliferation of injured neurons after treatment measured by EdU assay. (B) quantitative analysis for cell apoptosis of injured neurons after treatment measured by flow cytometry. (C) LDH content in injured neurons after treatment. (D) protein expression of NLRX1 and apoptosis-related factors (Bcl-2, Bax and Caspase-3) in injured neurons after treatment measured by Western blot analysis. * p < 0.05 compared with the treatment of sh-NC. # p < 0.05 compared with the treatment of oe-NKILA + sh-NC. & p < 0.05 compared with the treatment of miR-195 inhibitor + sh-NC. All data were measurement data and expressed as mean ± standard deviation. Unpaired t test was used for comparison between two groups. The one-way ANOVA was used for comparison among multiple groups, followed by Tukey’s post-hoc test. The cell experiment was repeated three times.