Canola oil is often promoted as a low-cost alternative to olive oil, possessing the same health benefits. It’s even promoted as having a mere 7% saturated fat, compared to olive oil’s 15%. But what does science say about the healthfulness of canola? Until recent years, no data were available on the effect of canola oil intake in relation to increasingly common diseases, like Alzheimer’s disease. Canola oil had never been examined as a causal factor in the sixteen-fold increase in deaths from Alzheimer’s reported in 1991: a total of 14,112, up from just 857 deaths reported in 1979.
In December 2017, researchers from Alzheimer’s Center at Temple University investigated the effect of daily consumption of canola oil on mice whose brains had developed both plaques and tangles, common brain characteristics for Alzheimer’spatients. Mice in the control group received a typical diet, while mice in the experimental group were fed a diet supplemented with canola oil for a period of 6 months. At the beginning of the study, mice had the same body weight. They were put through three different tests involving memory functions and conditioning, such as mazes. Ability to navigate these environments demonstrated measurable brain function and emotional stimulation.
PARP1/PAR depletion improved the cardiac structure and LV function in chagasic mice
ROS can signal fibrosis, and chronic hypertrophy is a key cause for LV dysfunction. We, therefore, examined if control of PARP1-dependent mitochondrial impairment and oxidative stress arrested cardiac remodeling and LV dysfunction in Chagas disease. Echocardiography imaging showed the LV mass and inter-ventricular septum thickness (IVS) were increased by 29–58%, while LV posterior wall (LVPW) was thinned by 31–47% in chagasic (vs. control) WT mice (Fig 6A–6E, all, p<0.05, S2 Table). Histological evaluation of tissue sections by Masson's Trichrome staining showed the myocardial collagen content was significantly increased in chagasic myocardium (score: 4.0 ± 0.4 vs. 0.3 ± 0.04, WT.Tc vs. WT, Fig 6F–6H, p<0.001). An increase in cardiac fibrosis in WT.Tc (vs. control) mice was also evidenced by 6-fold, 8-fold, and 1.5-fold increase in mRNA levels for COL1A1, COL3A1, and COL5A2, respectively (Fig 6I–6K, all, p<0.05). The chronically infected PARP1+/- and PARP1-/- mice exhibited the ability to maintain IVS and LVPW thickness at normal levels, >50% decline in collagen deposition, and 50–90% decline in the mRNA levels of collagen isoforms when compared to that noted in WT.Tc mice (Fig 6A–6K, all, p<0.05).
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