Hepatoprotection by curcumin and sulforaphane against tBHP-induced oxidative damage

Abstract

Background and aim: Antioxidants have recently been of keen therapeutic interest, due to the causative role of oxidative stress in induction and progression of liver, pancreatic and neurodegenerative diseases. Most plant-derived antioxidants are key components of vegetables and spices which are part of daily meals. Curcumin (from Asian spice turmeric) and sulforaphane (abundant in cruciferous vegetables such as broccoli), are reported to have antioxidant potential [1, 2] and were assessed in the current study for their cytoprotective activity in HepG2 liver cells. Methods: Radical scavenging activities of curcumin and sulforaphane were investigated against 2,2-diphenyl-1-picrylhydrazyl (DPPH). Using HepG2 liver cells, cytoprotection against tert-butyl hydroperoxide (tBHP)-induced cytotoxicity was evaluated in 5h co-exposure and 20h pre-exposure protocols with phytochemicals. Cell viability was determined in Neutral Red assay. Quercetin served as a positive phyto-antioxidant standard [3]. All phytochemicals were dissolved in DMSO to final solution of 10 mg/ml. Results and Discussion: Radical scavenging activity of quercetin was stronger than curcumin, but not significantly more potent in 5h co-exposure with tBHP. Sulforaphane was not cytoprotective in 5h protocol, this it lacked antiradical activity. Unlike quercetin, both phytochemicals were cytotoxic at high concentrations (Table 1). Conclusion: Sulforaphane, curcumin and quercetin could protect HepG2 cells via indirectly inducing intrinsic cytoprotective mechanisms during 20h pre-exposure protocol. Sulforophane does not act as a free radical scavenger, whilst curcumin and quercetin have antiradical properties, acting as direct and indirect antioxidants. The cytoprotective activities of quercetin, curcumin and sulforaphane suggest that these may be strong therapeutic phyto-antioxidants in preventing oxidative damage. Keywords: Curcumin, Antioxidant, Quercetin, Sulforaphane, HepG2