Autophagic Cell Death in Glioma Cell Induced by Ceramide through JNK/c-Jun Pathway / 中国康复理论与实践

Objective To observe the autophagy of 87-MG and U251 glioma cells induced by ceramide and explore the possible mecha-nism. Methods The viability and apoptosis of 87-MG and U251 cells were detected by MTT assay and flow cytometry, respectively. Autoph-agic-related protein expressions of LC3B/LC3A and Beclin-1 were determined by Western blotting. The activation of JNK/c-Jun signaling pathway induced by ceramide with or without the treatment of JNK specific inhibitor SP600125 was also measured. Results 24 hours after treatment of ceramide, the growth of 87-MG and U251 cells was significantly inhibited time-dependently (P<0.05);and the number of au-tophagic cells increased dose-dependently (P<0.05). The levels of LC3B/LC3A and Beclin-1 significantly increased after ceramide treat-ment (P<0.05). JNK signaling pathway was activated in the 87-MG and U251 cells and the phosphorylation of c-Jun also increased after ce-ramide treatment. This activation of autophagy could be reversed by the pre-treatment of SP600125. Conclusion Ceramide may induce au-tophagy in 87-MG and U251 glioma cells and the mechanism may be related to the activation of JNK/c-Jun signaling pathway.

Autophagic Cell Death in Glioma Cell Induced by Ceramide through JNK/c-Jun Pathway / 中国康复理论与实践

@#Objective To observe the autophagy of 87-MG and U251 glioma cells induced by ceramide and explore the possible mechanism. Methods The viability and apoptosis of 87-MG and U251 cells were detected by MTT assay and flow cytometry, respectively. Autophagic- related protein expressions of LC3B /LC3A and Beclin-1 were determined by Western blotting. The activation of JNK/c-Jun signaling pathway induced by ceramide with or without the treatment of JNK specific inhibitor SP600125 was also measured. Results 24 hours after treatment of ceramide, the growth of 87-MG and U251 cells was significantly inhibited time-dependently (P<0.05); and the number of autophagic cells increased dose-dependently (P<0.05). The levels of LC3B/LC3A and Beclin-1 significantly increased after ceramide treatment (P<0.05). JNK signaling pathway was activated in the 87-MG and U251 cells and the phosphorylation of c-Jun also increased after ceramide treatment. This activation of autophagy could be reversed by the pre-treatment of SP600125. Conclusion Ceramide may induce autophagy in 87-MG and U251 glioma cells and the mechanism may be related to the activation of JNK/c-Jun signaling pathway.