Table 2.

Examples of in vivo models of hepatoprotection using Nrf2 chemical activators.

Reference	Model	Result
Reddy et al., 1982	Dietary pretreament with BHA of mice exposed to methylazoxymethanol acetate	BHA decreased mortality and liver necrosis in mice exposed to methylazoxymethanol acetate
Hazelton et al., 1986	Dietary pretreament with BHA of mice exposed to acetaminophen	BHA decreased acetaminophen- induced hepatotoxicity and increased hepatic GSH and Ugt enzyme activity.
Kensler et al., 1987	Pretreament of rats with oltipraz exposed to aflatoxin	Oltipraz-treated rats had decreased hepatocarcinogenicity
Liu et al., 1993a	Pretreatment of mice with oleanolic acid exposed to acetaminophen	Oleanolic acid decreased acute liver injury, decreased glutathione conjugate formation, and increased glucuronide conjugate formation
Liu et al., 1993b	Pretreatment of mice with oleanolic acid exposed to cadmium	Oleanolic acid decreased liver injury.
Liu et al., 1994a	Pretreatment of mice with oleanolic acid exposed to various hepatotoxicants	Oleanolic acid decreased liver injury from carbon tetrachloride, cadmium, and acetaminophen, but not allyl alcohol
Liu et al., 1994b	Effect of 10 oleanane-type triterpenoid compounds on carbon tetrachloride, acetaminophen, and cadmium hepatotoxicity	Ursolic acid and oleanolic acid decreased liver injury from carbon tetrachloride, acetaminophen, and cadmium.
Liu et al., 1995a	Effect of oleanolic acid on chemical-induced liver injury in mice	Oleanolic acid protected from bromobenzene, acetaminophen, carbon tetracholoride, thioacetamide, furosemide, phalloidin, colchicine, cadmium chloride, and lipopolysaccharide
Wang et al., 1999	BHA pretreatment of rats with hepatitis B virus exposed to aflatoxin	BHA reduced hepatic carcinomas, adenomas and oxidative stress, while increasing Gst and Nqo1 activities.
Kensler et al., 2000	Oltipraz treatment of residents of China exposed to high dietary concentrations of aflatoxin	Reduction in the urinary excretion of the primary oxidative metabolite of aflatoxin B1, namely aflatoxin M1
Yates et al., 2006	CDDO-Im pretreatment of rats exposed to aflatoxin	CDDO-Im decreased aflatoxin adduct formation, hepatocarcinogenesis, and induced Gst and aflatoxin aldehyde reductase protein expression.
Osburn et al., 2008	CDDO-Im pretreatment of wild-type and Nrf2-null mice administered ConA	CDDO-Im protected wild-type but not Nrf2-null mice from ConA- induced inflammatory hepatic injury.
Tanaka et al., 2009	Oltipraz pre- and post- treated mice administered ANIT	Oltipraz protected mice from ANIT- induced cholestasis.
Reisman et al., 2009a	Oleanolic acid pretreatment of wild-type and Nrf2-null mice administered acetaminophen	Oleanolic acid protected wild-type mice more than Nrf2-null mice from acetaminophen-induced hepatotoxicity
Reisman et al., 2009b	CDDO-Im pretreatment of wild-type and Nrf2-null mice administered acetaminophen	CDDO-Im protected wild-type but not Nrf2-null mice from acetaminophen-induced hepatotoxicity
Shin et al., 2009	CDDO-Im treatment of wild- type and Nrf2-null mice given a high-fat diet	CDDO-Im reduced increases in body weight, adipose mass, and hepatic lipid accumulation in wild- type mice but not in Nrf2-null mice.