Title : Protective effect of the peroxisome proliferator-activated receptor (PPAR)-γ, ligand rosiglitazone on tert-butyl hydroperoxide-induced QZG cell injury.

Pub. Date : 2011 Sep

PMID : 20510595






4 Functional Relationships(s)
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1 Under 400 muM t-BHP treatment, QZG cell displayed significant loss of viability and dramatic morphological changes characterized by changing in shape from triangle to spherical, disappearance of cell cilia, swollen mitochondrial and typical apoptotic alteration such as condensation of chromatin, and appearance of crescent under light microscopy and electronic microscopy, respectively. tert-Butylhydroperoxide latexin Homo sapiens
2 25 muM rosiglitazone treatment inhibited the t-BHP-induced cell toxicity significantly by restoring the cell viability, reducing cell population undergone apoptosis to normal level (3.5%) and ameliorating t-BHP-induced pathological changes. tert-Butylhydroperoxide latexin Homo sapiens
3 25 muM rosiglitazone treatment inhibited the t-BHP-induced cell toxicity significantly by restoring the cell viability, reducing cell population undergone apoptosis to normal level (3.5%) and ameliorating t-BHP-induced pathological changes. tert-Butylhydroperoxide latexin Homo sapiens
4 Real-time RT-PCR results showed that 400 muM t-BHP caused dramatic down-regulation of PPARgamma expression in QZG cells, whereas combining treatment with 25 muM rosiglitazone resistant to PPARgamma expression to normal level partially. tert-Butylhydroperoxide latexin Homo sapiens