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Fig. 5. Schematic diagrams representing chrysin and DCA actions on GBMs. (A) Under normoxia, chrysin treatment suppresses the expression of HIF1α and the HIF1α target genes, GLUT1 and PDKs, and the inhibition of PDKs with DCA disinhibits PDH which provides the initial substrate for the TCA cycle in mitochondria. (B) Under hypoxia, GBMs express high levels of HIF1α and the glycolysis-regulating genes, GLUT1 and PDKs, which promote hypoxia-mediated increase of cell viability along with an increase of glycolytic adaptation. Thus, hypoxia-dependent resistance was sustained in all cell types, and chrysin and DCA co-treatment was ineffective in eliminating this resistance.
Exp Neurobiol 2017;26:295~306
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