Betulinic acid inhibits glioma cell viability by downregulation of NF-?B and enhancement of apoptosis

Purpose: To determine the inhibitory potential of betulinic acid on pro-survival signaling pathway in glioblastoma.Methods: Changes viabilities glioma cells and primary astrocytes were measured using 3-(4, 5dimethylthiazol-2-yl)-2, 5-diphenyltetrazolium bromide (MTT) assay. Apoptotic changes analyzed Hoechst 33342 staining Annexin V-FITC/PI kits. Western blotting was used for assaying protein expressions various pro-apoptotic anti-apoptotic factors.Results: The proliferative U87MG A172 significantly reduced treatment with a concentration- time-dependent manner. Treatment at dose 8.75 µg/mL increased apoptosis to 41.8 ± 0.5 48.8 0.5%, respectively (p < 0.05). Betulinic decreased intracellular levels NF?B p65 andsuppressed survivin, XIAP Bcl-2 However, Bax activated caspase-9 caspase-3 0.05).Conclusion: inhibited proliferation glioblastoma mediated their apoptosis. There is need vivo studies validation therapeutic as an anti-glioblastoma drug.
 Keywords: Glioblastoma, acid, Proliferation, Apoptosis, Chemotherapy, Intracranial malignancy