These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.


Pubmed for Handhelds

PUBMED FOR HANDHELDS

Search MEDLINE/PubMed

  • Title: The protection of NF-κB inhibition on kidney injury of systemic lupus erythematosus mice may be correlated with lncRNA TUG1.
    Author: Cao HY, Li D, Wang YP, Lu HX, Sun J, Li HB.
    Journal: Kaohsiung J Med Sci; 2020 May; 36(5):354-362. PubMed ID: 31930775.
    Abstract:
    We aimed to know the effect of nuclear factor-kappa B (NF-κB) inhibition on the kidney injury of systemic lupus erythematosus (SLE) mice. Pristane-induced SLE mice were treated with pyrrolidine dithiocarbamate (PDTC, 50 or 100 mg/kg), a NF-κB inhibitor. Histopathological changes were observed by hematoxylin & eosin, Masson and periodic schiff-methenamine stainings. Long noncoding RNA Taurine upregulated gene 1 (LncRNA TUG1) was measured by real-time reverse transcription PCR, NF-κB p65 expression by western blotting, levels of inflammatory cytokines, antinuclear antibodies (ANA), and antidouble stranded DNA (anti-dsDNA) by enzyme-linked immunosorbent assay, and the deposition of IgG and C3 by immunofluorescence. The kidney of SLE mice exhibited interstitial inflammatory cell infiltration, interstitial fibrous proliferation, glomerular mesangial proliferation, and crescent formation, which was mitigated after PDTC administration. The levels of BUN, Cr, ANA, and anti-dsDNA and the pro-inflammatory factors in SLE mice were increased with obvious deposition of IgG and C3, but they were also reversed by PDTC. Furthermore, the NF-κB p65 expression in the nucleus in the SLE mice was decreased with the up-regulation of TUG1 expression and NF-κB p65 expression in the cytoplasm after PDTC treatment. Correlation analysis revealed the negative correlation between the TUG1 expression and NF-κB p65 in the nucleus in the kidney tissues. NF-κB inhibition with PDTC protected against the kidney injury of pristine-induced SLE mice possibly via up-regulating lncRNA TUG1, and further clinical studies are needed to clarify whether NF-κB inhibition may be a therapeutic modality for the kidney injury of SLE.
    [Abstract] [Full Text] [Related] [New Search]