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

NKILA promotes proliferation and inhibits apoptosis of injured neurons. The injured neurons were introduced with oe-NKILA, sh-NKILA, vector or sh-NC. (A) NKILA expression in injured neurons after treatment measured by RT-qPCR. (B) cell proliferation of injured neurons after treatment measured by EdU assay. (C) quantitative analysis for cell apoptosis of injured neurons after treatment measured by flow cytometry. (D) LDH content in injured neurons after treatment. (E) protein expression of apoptosis-related factors (Bcl-2, Bax and Caspase-3) in injured neurons after treatment measured by Western blot analysis. * p p

Figure 2. NKILA promotes proliferation and inhibits apoptosis of injured neurons. The injured neurons were introduced with oe-NKILA, sh-NKILA, vector or sh-NC. (A) NKILA expression in injured neurons after treatment measured by RT-qPCR. (B) cell proliferation of injured neurons after treatment measured by EdU assay. (C) quantitative analysis for cell apoptosis of injured neurons after treatment measured by flow cytometry. (D) LDH content in injured neurons after treatment. (E) protein expression of apoptosis-related factors (Bcl-2, Bax and Caspase-3) in injured neurons after treatment measured by Western blot analysis. * p < 0.05 compared with neurons treated with vector; # p < 0.05 compared with neurons treated with sh-NC. All data were measurement data and expressed as mean ± standard deviation. One-way ANOVA was used for comparison among multiple groups, followed by Tukey’s post-hoc test. The cell experiment was repeated three times.