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. Author manuscript; available in PMC: 2014 Nov 4.
Published in final edited form as: Basic Clin Pharmacol Toxicol. 2007 Oct;101(4):262–268. doi: 10.1111/j.1742-7843.2007.00116.x

Fig. 4.

Fig. 4

Protective effect of silymarin on palmitate-induced cell death is independent of its antioxidant property. (A) Changes of intracellular malondialdehyde (MDA) + 4-hydroxyalkenals (HAE) content (μM). HepG2 cells were incubated with 0.25 mM palmitate for 20 hr with or without silymarin or N-acetylcysteine (NAC) pre-treatment. (B) Changes of intracellular glutathione (GSH) content (nmol/million cells). HepG2 cells were incubated with 0.25 mM palmitate for 4 and 8 hr, respectively, with or without silymarin or N-acetylcysteine (NAC) pre-treatment. *Value is significantly different from that seen in the presence of palmitate alone, P < 0.05. (C) NAC did not protect palmitate-induced cell death in HepG2 cells. Apoptosis was measured by DNA fragmentation ELISA assay and expressed as fold of untreated. Values in bars that do not share a letter differ significantly. (D) Changes of 2′,7′-dichlorohydrofluorescein diacetate fluorescent products. HepG2 cells were incubated with 300 μM H2O2 for 1 hr or with palmitate for 1, 4 and 20 hr, respectively. Data are expressed as Arbitrary Fluorescence Units. *Value is significantly different from that seen in the control cells, P < 0.05. At least three experiments were conducted for each measurement.