Close
  Indian J Med Microbiol
 

Figure 2: Betulinic acid chalcone suppressed rosiglitazone persuaded (a) peroxisome proliferator-activated receptor-γ-ligand-binding domain activation and (b) PPRE-Luc transcription in 293T cells. The cell line 293T UAS-TK-Luc comprising an integrated reporter in which the luciferase gene is under the control of Gal4-binding site (UAS) upstream of the thymidine kinase promoter was employed. The cells were transfected with plasmids for peroxisome proliferator-activated receptor-γ-ligand-binding domain and pRL-SV40 (reference) followed by incubation with betulinic acid chalcone at 6 h of transfection. The luciferase activity was investigated at 24 h of betulinic acid chalcone treatment using the kit luciferase. Data are accessible as the means ± standard deviation (n = 6) (*P < 0.01 and **P < 0.001 vs. control group)

Figure 2: Betulinic acid chalcone suppressed rosiglitazone persuaded (a) peroxisome proliferator-activated receptor-γ-ligand-binding domain activation and (b) PPRE-Luc transcription in 293T cells. The cell line 293T UAS-TK-Luc comprising an integrated reporter in which the luciferase gene is under the control of Gal4-binding site (UAS) upstream of the thymidine kinase promoter was employed. The cells were transfected with plasmids for peroxisome proliferator-activated receptor-γ-ligand-binding domain and pRL-SV40 (reference) followed by incubation with betulinic acid chalcone at 6 h of transfection. The luciferase activity was investigated at 24 h of betulinic acid chalcone treatment using the kit luciferase. Data are accessible as the means ± standard deviation (<i>n </i>= 6) (*<i>P </i>< 0.01 and **<i>P </i>< 0.001 vs. control group)