Skip to main content

Advertisement

Fig. 6 | Journal of Experimental & Clinical Cancer Research

Fig. 6

From: Celastrol mediates autophagy and apoptosis via the ROS/JNK and Akt/mTOR signaling pathways in glioma cells

Fig. 6

Celastrol induced ROS generation, phosphorylation of JNK and interrupted the Akt/mTOR signaling pathway in glioma cells. a, b and c Glioma cells were treated with 3 μM celastrol in the presence or absence of NAC (5 mM) or SP (40 μM) for 12 h. Cells were stained with 10 μM DCFH-DA at 37 °C in the dark for 20 mins, and the ROS level was determined by fluorescence microscopy and flow cytometry. Quantitative analysis of ROS generation was shown in histograms. Scale bars = 200 μm. d U251 cells were treated with various concentrations of celastrol for 24 h or incubated with celastrol (3 μM) for different durations. The expression levels of p-JNK, JNK, p-p38, p38, p-Akt, Akt, p-mTOR and mTOR were detected by western blotting. β-actin was used as an internal control. Data are presented as the Mean ± SD (n = 3). **P < 0.01, ***P < 0.001, versus control, ###P < 0.001, versus celastrol treatment group

Back to article page