Taken together, GSH concentrations in the liver, the mRNA for the GSH conjugation and peroxide-reduction enzymes, and the mRNA for ratelimiting enzyme for GSH synthesis Gclc were expressed at Kaempferide higher levels with graded Nrf2 activation in the Nrf2 “genedose” model, not only at basal levels, but also at much higher levels after microcystin challenge. Thus, enhancement of GSH synthetic, conjugating and peroxide reduction enzymes appear to be important for reducing inflammation and oxidative stress in mice with genetic Ursolic-acid over-expression of Nrf2. In conclusion, the present study demonstrates that Nrf2 activation decreases microcystin-induced oxidative stress and liver injury. The protective effects of Nrf2 appear to depend on higher expression of genes involved in antioxidant defense, particularly the enhanced GSH synthetic, conjugation and peroxide reduction enzymes. Atherosclerosis risk increases with age and unhealthy nutritional habits during childhood and youth have been suggested to favor atherosclerosis complications later in life. Longitudinal cohort studies have demonstrated increased cardiovascular risk in adulthood of obese children and that exposure to cardiovascular risk factors early in life may contribute to the development of atherosclerosis.The increasing consumption of cola beverages has been associated with obesity and a rising incidence of atherosclerosis and cardiovascular disease over the past decades. We have reported the development of metabolic syndrome after long-term cola beverages consumption in rats. Hypertension, hyperglycemia, increased body weight, dyslipidemia and echocardiographic alterations were observed while pathology findings were scarce, related to aging rather than treatment. Recently we observed that ApoE2/2C57BL/6J mice exhibited a particular sensitivity to the effects of cola beverage drinking. Arterial pathology was induced bysucrosesweetened cola drinking in association with hyperglycemia. Rate of progression of atherosclerotic lesions was higher in C and L groups compared with W group over the time of the study. Macrophages and myofibroblasts participated in the pathological process while no proliferative activity was found. The observed increase in foamy Mo population in atherosclerotic plaque in ApoE2/2 mice might be favored by the characteristic endothelial dysfunction described in this model. During the wash-out period, Mo population decreased likely due to necrosis leading to formation of the large globular accumulations of extracellular lipids observed in 30 week-old mice. At the same time Mo-induced Mf migration into the plaque might contribute with collagen synthesis to fibro fa y nodules formation.Endothelial dysfunction typically observed in ApoE2/2 mice is suggested to play a major role in atherosclerotic plaque formation in this mice model long after soft drinks consumption. Several studies have demonstrated endothelial dysfunction in different vascular beds in ApoE2/2 mice and the negative influence of high fat high carbohydrate diets on endothelial function has been confirmed in this mice model. In our analysis, although the pathological sequence leading to atherosclerotic plaque formation was common to all experimental groups, plaque/media-ratio was higher in mice that had consumed cola drinks.