Increased susceptibility of renal epithelial cells to TNFα-induced apoptosis following treatment with fumonisin B1

摘要: Previous studies have shown that tumor necrosis factor alpha (TNFalpha) is involved in the pathogenic events following exposure to fumonisin B(1) (FB(1)), a potent inhibitor of ceramide synthase and sphingolipid biosynthesis. The intimate role mediators TNFalpha signaling cellular death suggests FB(1) may alter sensitivity cells TNFalpha-induced apoptosis. We tested hypothesis treatment will increase porcine renal epithelial TNFalpha. Porcine (LLC-PK(1)) were treated with for 48 h prior A dose-dependent apoptosis was observed pretreated FB(1). Cells showed increased DNA fragmentation terminal uridine nucleotide end labeling response treatment. synthesis resulted cell cycle arrest G(2)/M phase cycle. Flow cytometric analysis indicated predominantly killed phase. activation JNK, mitogen-activated protein kinase (MAPK), Phosphorylation p38 ERK remained unchanged also free sphingoid base levels under identical conditions. Results suggest population This be most susceptible pro-apoptotic JNK play an important these effects.