ABSTRACT
AIM: To explore the effect of microRNA-146a (miR-146a) on apoptosis of human gastric cancer SGC-7901 cells and the underluing mechanism.METHODS: miR-146a mimic (up-regulated miR-146a expression) and miR-146a inhibitor (down-regulated miR-146a expression) were transfected into the SGC-7901 cells by liposome method.At the same time, miRNA nonsense sequence transfection group as the negative control group (NC group) was set up.RT-qPCR was used to evaluate the levels of miR-146a in the SGC-7901 cells after transfection.The effects of miR-146a on the cell apoptosis and growth were assessed by flow cytometry analysis and CCK-8 assay, respectively.The effect of over-expression or knockdown of miR-146a on transforming growth factor-β-activated kinase 1 (TAK1)/ nuclear factor-kappa B (NF-κB) signaling was evaluated by RT-qPCR and Western blot.RESULTS: miR-146a modulated apoptosis of SGC-7901 cells.Over-expression of miR-146a significantly increased apoptosis, whereas knockdown of miR-146a inhibited the apoptosis of SGC-7901 cells.The expression of TAK1 at mRNA and protein levels was significantly decreased when miR-146a mimic was transfected into the SGC-7901 cells (P<0.05).On the contrast, the expression of TAK1 at mRNA and protein were significantly higher in miR-146a inhibitor transfection group than that in NC group (P<0.05), suggesting that miR-146a negatively regulated TAK1 expression.Moreover, knockdown of TAK1 enhanced the apoptosis of SGC-7901 cells (P<0.01), while over-expression of TAK1 inhibited the apoptosis of SGC-7901 cells(P<0.01).Additionally, both over-expression of miR-146a and knockdown of TAK1 led to a prominent increase in the expression of NF-κB inhibitor protein alpha (IκBα) and a significat decrease in B cell lymphoma-2 (Bcl-2) level in the SGC-7901 cells.CONCLUSION: miR-146a significantly promotes apoptosis of SGC-7901 cells by inhibition of NF-κB pathway via targeting TAK1.
ABSTRACT
Objective To elevate the efficacy and safety of descending neurogenic evoked potentials (DNEP) monitoring during severe rigid spinal deformity surgery.Methods All of 108 patients (43 males,65 females) who underwent surgical treatment for spinal deformity in our spinal center from July 2010 to August 2013 were retrospectively reviewed.The average age (17.5±5.8) ys(range 12-50 ys),the average following period is 38.6 months(range 24-52 months).Combined monitoring of SEP,MEP and DNEP model were used during surgery.All subjects with no neurological deficits preoperatively and got satisfied outcomes.Respectively evaluate the results of neurophysiological intraoperative monitoring (IOM).Data were collected to elevate the efficacy and safety of DNEP monitoring.Results All of 108 patients,15 patients (13.9％,15/108) showed significant changes of neurophysiological parameters,of which 9 cases (60％,9/15) were identified as true positive and 6 cases (40％,6/15) were identified as false positive.During the following-up period,2 patients developed permanent neurological deficit,and 3 patients showed transient neurological deficit who got fully recovered within 6 months after operation.DNEP showed alert in all 5 patients with truepositive alarm,of which 2 patients developed permanent neurological dysfunction and 3 cases showed postoperative short nerve dysfunction that got fully recovery within 6 months after operation.The sensitivity and specificity of SEP+MEP and DNEP were 100％ and 97.98％,100％ and 98.99％,respectively.Conclusion Combining use of MEP+SEP+DNEP monitoring during surgical treatment of spinal deformities presented to be a highly reliable method for the detection and prevention of iatrogenic injury.The results confirmed a high efficacy and safety of DNEP monitoring during spinal surgery.