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A Novel Model of Mild Traumatic Brain Injury for Juvenile Rats
Published on: December 8, 2014
Expression of NF-κB in juvenile rats with nephrotic syndrome and its effects on inflammatory changes and renal injury
1Department of Pediatrics, West China Second University Hospital, Sichuan University, Chengdu, China. wangdo620@163.com.
Objective:
The aim of this study was to investigate the expression of nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) in juvenile rats with nephrotic syndrome, and to explore its effects on inflammatory changes and renal injury.
Materials And Methods:
24 Sprague-Dawley (SD) rats were randomly divided into the normal group (n=12) and model group (n=12). Rats in the normal group were intraperitoneally injected with normal saline. Meanwhile, rats in the model group were given azithromycin hydrochloride injection to establish the model of nephrotic syndrome. After 24 h of modeling, the samples were collected. The expression of NF-κB was detected via immunohistochemistry. Moreover, the protein expression of NF-κB was determined through Western blotting. Quantitative Polymerase Chain Reaction (qPCR) was used to measure the messenger ribonucleic acid (mRNA) expression levels of interleukin-1 (IL-1) and IL-6. Meanwhile, the content of IL-1 and IL-6 was detected by enzyme-linked immunosorbent assay (ELISA). The serum levels of urea nitrogen and serum creatinine were measured by an automatic biochemical analyzer. Furthermore, the correlation between NF-κB protein with IL-1 and IL-6 were studied via Pearson analysis.
Results:
Compared with the normal group, rats in the model group exhibited significantly increased expression and protein expression of NF-κB (p<0.05). Meanwhile, the mRNA expression levels and content of IL-1 and IL-6 (p<0.05), as well as the serum levels of urea nitrogen and creatinine (p<0.05) of the model group were markedly higher than those of the normal group. Furthermore, NF-κB protein was positively correlated with IL-1 and IL-6 contents.
Conclusions:
NF-κB is highly expressed in juvenile rats with nephrotic syndrome, which promotes the expressions of inflammatory factors (IL-1 and IL-6) and aggravates the renal injury.
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