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10-Dehydrogingerdione raises HDL-cholesterol through a CETP inhibition and wards off oxidation and inflammation in dyslipidemic rabbits
Update time:2013-11-07 00:07:05   【 Font: Large  Medium Small



To investigate the CETP suppression by 10-dehydrogingerdione, a compound in Zingiber officinale, and its effect on the progression of atherosclerosis in dyslipidemic rabbits and the underlying oxidative and inflammatory consequences.


Twenty-four New Zealand male rabbits were fed either a normal diet or an atherogenic diet. The rabbits on the atherogenic diet received treatments of atorvastatin or 10-dehydrogingerdione and placebo concurrently (n = 6/group). Blood samples were collected after three and six weeks for biochemical analysis.


10-Dehydrogingerdione-treated rabbits showed a significant improvement in serum lipids especially HDL-C in a time-dependant manner. This effect was correlated to its ability to lower CETP. Lp(a), ox-LDL, hsCRP, homocysteine and MMP9 decreased significantly in both 10-dehydrogingerdione- and atorvastatin-treated rabbits compared with placebo (p < 0.001). Lp(a) achieved normal values by both treatments, while homocysteine did not reach normal values by either treatments. Conversely, MMP9 returned below normal values by 10-dehydrogingerdione (p < 0.001), hsCRP and ox-LDL were slightly below normal values (hsCRP:p < 0.001; ox-LDL: p < 0.001 and p < 0.05 in 10-dehydrogingerdione and atorvastatin groups, respectively). The effect achieved by 10-dehydrogingerdione was similar to that of atorvastatin on hsCRP and Lp(a). However, 10-dehydrogingerdione exerted better effect than atorvastatin on homocysteine, MMP9 (p < 0.001) and ox-LDL (p < 0.05).


In a rabbit dyslipidemic model, 10-dehydrogingerdione lowers LDL-C and raises HDL-C by suppressing CETP; an effect that modulates inflammatory and oxidative risk factors of CVD. These findings suggested that the naturally occurring 10-dehydrogingerdione might be a potential CETP inhibitor for the treatment of atherosclerosis and residual risk in CVD.

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Source:Atherosclerosis      by Mohamed M. Elseweidy,Fatma R. Abdallah, Nahla N. Younis,Sameih Aldohmy, Haitham M. Kassem
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