Abstract:

Objective: The protective role of ethanol extract of Boschniakia rossica (BREE) against cellular oxidative injury
induced by hydrogen peroxide (H2O2) in HepG2 cell line was investigated. Methods: MTT assay was used to e valuate the
cell proliferation of HepG2 cells. The activities of lactate dehydrogenase (LDH), alanine aminotransferase (ALT), aspartate
aminotransferase (AST), malondialdelyde (MDA), superoxide dismutase (SOD) and reduced glutathione (GSH) were
measured by the spectrophotometric method. The total protein expression and the phospharylation of extracellular signalregulated
kinase (ERK), c-Jun N-terminal kinase (JNK), p38 mitogen-activated protein kinase (p38 MAPK), and nuclear
translocation of nuclear factor-κB (NF-κB) were determined by the Western blotting method. Results: BREE had no toxic
effect on cultured HepG2 cells at the tested concentrations. In HepG2 cells with H2O2-induced oxidative damage, BREE
increased cell viability, reduce LDH, ALT and AST leakage, inhibited MDA formation, and increased SOD and GSH levels.
At the different stages of oxidative damage, ERK, JNK, p38 MAPK and NF-κB proteins were activated; however, the
administration of BREE suppressed the ERK activation and NF-κB nuclear translocation at 1 h, and JNK activation at 12 h.
Conclusion: BREE can function as an antioxidant to prevent cellular injury induced by H2O2 in cultured HepG2 cells, maybe
via the suppression of ERK and JNK activation and NF-κB nuclear translocation.

Key words: Boschniakia rossica, hydrogen peroxide (H2O2), oxidative damage, HepG2 cell