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. 2004 Nov 9;384(Pt 1):149–157. doi: 10.1042/BJ20040928

Figure 3. Blocking PPARγ activation abrogates the pro-apoptotic effects of curcumin on activated HSC in vitro.

Figure 3

Passaged HSC were pretreated or not with the specific PPARγ antagonist PD 68235 (10 or 20 μM) for 30 min prior to the addition of curcumin (Cur.; 20 μM) for an additional 24 h. Total RNA or whole-cell protein extracts were prepared. (A) Real-time PCR. GAPDH was used as an invariant control for calculating fold changes in mRNA levels (n=3). Values are expressed as means±S.D. Significance: *P<0.05 compared with cells with no treatment; †P<0.05 compared with cells treated only with curcumin. (B) Western blotting analyses. β-Actin was an internal control for equal loading (n=3). (C) Caspase 3 activity assays. Values are expressed as means±S.D. (n=3 independent experiments). Significance: *P<0.05 compared with cells with no treatment; ‡P<0.05 compared with cells treated only with curcumin.