The study of the differential gene expression profiles related to toxic effects in rats exposed to silica.
- Author:
Ping LIU
1
;
Le CHEN
;
Wei LIU
;
Hai-xia KONG
;
Shi-xin WANG
;
Zhi-guang TU
Author Information
- Publication Type:Journal Article
- MeSH: Animals; Lung; drug effects; metabolism; Male; Oligonucleotide Array Sequence Analysis; Pulmonary Fibrosis; chemically induced; genetics; metabolism; Rats; Rats, Wistar; Silicon Dioxide; toxicity; Transcriptome
- From: Chinese Journal of Industrial Hygiene and Occupational Diseases 2011;29(11):806-811
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo study the differential gene expression profiles related to toxic effects in rats exposed to silica.
METHODSWistar rats exposed to SiO2 (50 mg/ml) and 1 ml normal saline by intratracheal injection served as the exposure and control groups, on the 14th day after exposure all rats were executed and the rat lung tissues were obtained. The differential gene expression profiles in the lung tissues of rats exposed to silica were detected using confocal fiber beads gene chip technique, and the differential expression profiling data were analyzed using the database for annotation, visualization and integrated discovery (DAVID) bioinformation analysis tool.
RESULTSThe results of present study indicated that 1567 genes with differential expression were identified in 22107 genes of rat lung tissues in exposure group, including 765 up-regulated genes and 802 down-regulated genes as compared to control group. In the 461 genes related to toxic effects, 285 genes were up-regulated and 176 genes were down-regulated in exposure group. The trends of up-regulation of HMOX1 and SOD2 genes in RT-PCR assay were similar to those in gene chip technique.
CONCLUSIONA large number of genes related to toxic effects in the rats with silica-induced pulmonary fibrosis appeared up-regulation or down-regulation. There may be a complex gene regulation network in the pulmonary fibrosis induced by SiO2, and the toxicological mechanism is an important part in the development of pulmonary fibrosis.