title: Effect of Salvia miltiorrhiza on aflatoxin B1-induced oxidative stress in cultured rat hepatocytes.
abstract: Recent findings have suggested that oxidative damage might contribute to the cytotoxicity and carcinogenicity of aflatoxin B1 (AFB1). Salvia miltiorrhiza (Sm), a herbal plant that has been used extensively in traditional Chinese medicine for treating cardiovascular and liver diseases, is believed to have some antioxidative capabilities. In this study, the protective effect of Sm against AFB1-induced cytotoxicity was investigated in cultured primary rat hepatocytes. AFB1-induced cytotoxicity and lipid peroxidation (LPO) were estimated by determination of lactate dehydrogenase (LDH) leakage and thiobarbituric acid reactive substances (TBARS) formation, respectively. Intracellular reactive oxygen species (ROS) formation was measured using a fluorescent probe 2',7'-dichlorofluorescein diacetate (DCFH-DA). In addition, changes of intracellular glutathione (GSH) content were also studied. Results showed that Sm was able to suppress the LDH leakage induced by AFB1 in a dose-dependent manner. A dose-dependent inhibitory effect of Sm on AFB1-induced LPO was also found in hepatocytes treated with Sm. It was further observed that Sm produced an inhibitory effect on ROS formation caused by AFB1. Concomitantly, the GSH content in Sm-treated groups increased substantially compared to those without Sm treatment. These findings suggest that Sm can inhibit the cytotoxicity of AFB1 through decreasing ROS formation, inhibiting LPO and preventing GSH depletion. The major component of the aqueous extract of Sm was identified by using high performance liquid chromatography (HPLC), proton magnetic resonance (1H-NMR) and mass spectrum (MS). Analytical results suggested that D(+)beta3,4-dihydroxyphenol lactic acid (DA) is the main compound of the aqueous extract of Sm.
authors.affiliation: Department of Community, Occupational and Family Medicine, Faculty of Medicine, National University of Singapore, Republic of Singapore.
authors.forename: J
authors.initials: J
authors.lastname: Liu
authors.forename: C F
authors.initials: CF
authors.lastname: Yang
authors.forename: B L
authors.initials: BL
authors.lastname: Lee
authors.forename: H M
authors.initials: HM
authors.lastname: Shen
authors.forename: S G
authors.initials: SG
authors.lastname: Ang
authors.forename: C N
authors.initials: CN
authors.lastname: Ong
mesh_terms: D016604:Aflatoxin B1 / Q000494:pharmacology*; D000818:Animals; D002478:Cells, Cultured; D002851:Chromatography, High Pressure Liquid; D004365:Drugs, Chinese Herbal / Q000737:chemistry / Q000494:pharmacology*; D005978:Glutathione / Q000378:metabolism; D007770:L-Lactate Dehydrogenase / Q000187:drug effects / Q000378:metabolism; D007773:Lactates / Q000737:chemistry / Q000302:isolation & purification / Q000494:pharmacology; D019686:Lamiaceae / Q000737:chemistry; D015227:Lipid Peroxidation / Q000187:drug effects; D008099:Liver / Q000166:cytology / Q000187:drug effects* / Q000378:metabolism*; D008297:Male; D018384:Oxidative Stress / Q000187:drug effects*; D051381:Rats; D011916:Rats, Inbred F344; D017382:Reactive Oxygen Species / Q000378:metabolism; D017392:Thiobarbituric Acid Reactive Substances / Q000032:analysis / Q000378:metabolism
chemical_list: D004365:Drugs, Chinese Herbal; D007773:Lactates; D017382:Reactive Oxygen Species; D017392:Thiobarbituric Acid Reactive Substances; C070324:alpha-(3,4-dihydroxyphenyl)lactic acid; D016604:Aflatoxin B1; D007770:L-Lactate Dehydrogenase; D005978:Glutathione