Details

Autor(en) / Beteiligte

• Wang, Cuifen
• Dai, Xiaoniu
• Liu, Hua
• Yi, Hongwei
• Zhou, Dongrui
• Liu, Chunhui
• Ma, Min
• Jiang, Zhenzhou
• Zhang, Luyong

Titel

Involvement of PPARγ in emodin-induced HK-2 cell apoptosis

Ist Teil von

• Toxicology in vitro, 2015-02, Vol.29 (1), p.228-233

Ort / Verlag

England: Elsevier Ltd

Erscheinungsjahr

2015

Link zum Volltext

Quelle

MEDLINE

Beschreibungen/Notizen

• •Emodin induced caspase 3 cleavage and activation in HK-2 cells.•Emodin decreased the mitochondrial membrane potential.•Emodin increased the release of cytochrome c from mitochondria.•Emodin upregulated PPARγ mRNA and protein expression.•Emodin enhanced the stability of PPARγ mRNA. Emodin, a major compound in total rhubarb anthraquinones (TRAs), has exhibited nephrotoxicity in Sprague Dawley rats and cytotoxicity to HK-2 cells, a human proximal tubular epithelial cell line, in our previous study. However, the exact molecular mechanisms underlying emodin-induced cytotoxicity remain undefined. In this study, the exposure of HK-2 cells to emodin led to decreased cell viability, caspase 3 cleavage and activation, loss of mitochondrial membrane potential (ΔΨm), and cytochrome c release from mitochondria to cytosol. Meanwhile, the levels of peroxisome proliferator-activated receptor gamma (PPARγ) mRNA and protein expression were elevated. GW9662, an antagonist of PPARγ, dramatically ameliorated the release of cytochrome c, the activation of caspase 3, and the reduction of cell viability induced by emodin. Importantly, emodin at the concentration causing apoptosis enhanced the stability of PPARγ mRNA. Taken together, these findings suggest that PPARγ might mediate, at least in part, emodin-induced HK-2 cell apoptosis via mitochondrial pathway.