Effect of knockdown of long noncoding RNA metastasis associated lung adenocarcinoma transcript 1 on microglial activation
10.3760/cma.j.issn.1671-8925.2018.05.003
- VernacularTitle:下调长链非编码RNA MALAT1表达对小胶质细胞活化的影响
- Author:
Junling ZHANG
1
;
Haiying PAN
;
Min XU
;
Xiaoyun LI
;
Jianyi NIU
Author Information
1. 262500,潍坊市益都中心医院神经内科
- Keywords:
Metastasis associated lung adenocarcinoma transcript 1;
Microglial cells;
Inflammatory reaction;
NF-κB signaling pathway;
Long noncoding RNA
- From:
Chinese Journal of Neuromedicine
2018;17(5):445-449
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the effect of down-regulation of human lung adenocarcinoma metastasis-associated transcript 1 (MALAT1) on microglial activation and its possible mechanism.Methods BV2 microglial cells were cultured in vitro and divided into a normal control group (no treatment),a lipopolysaccharide (LPS) treatment group (cultured with 100 ng/mL LPS),a MALAT1 interference group (transfected with MALAT1 interference sequence + cultured with 100 ng/mL LPS) and a control sequence group (transfected with control sequence + cultured with 100 ng/mL LPS).Real-time fluorescence quantitative PCR was used to detect the expression ofMA LA T1 mRNA in the cells.Western blotting was used to detect the expression of NF-κB protein and IκB-α protein in the cells.Enzyme linked immunosorbent assay (ELISA) was used to detect the levels of IL-1β,IL-6,IL-10 and TNF-α in each group.Nitric acid reduction method (Griess method) was used to detect nitric oxide (NO) concentration in each group.Results The relative expression levels of MALA T1 mRNA and NF-κB protein were significantly increased,the relative expression level of IκB-α protein was significantly decreased,the levels ofIL-1β,IL-6,IL-10 and TNF-α and the release of NO in the cell supernatant were significantly increased in the LPS treatment,MALAT1 interference and control sequence groups than in the normal control group (P＜0.05).The relative expression levels of MALAT1 mRNA and NF-κB protein were significantly decreased,the expression level of IκB-α protein was significantly increased,the levels ofIL-1β,IL-6,IL-10 and TNF-α and the release of NO in the cell supematant were significantly decreased in the MALAT1 interference group than in the LPS treatment and control sequence groups (P＜0.05).Conclusions Down-regulation of MALA T1 gene expression may inhibit the inflammatory response induced by LPS-induced BV2 cell activation.The mechanism might be related to the inhibition of NF-κB signaling pathway.
