The class
10-Dehydrogingerdione raises HDL cholesterol by suppressing CETP and curbs oxidative and inflammatory markers in rabbits (Atherosclerosis 2013)
Original title: 10-Dehydrogingerdione raises HDL-cholesterol through a CETP inhibition and wards off oxidation and inflammation in dyslipidemic rabbits
Researchers tested whether 10-dehydrogingerdione, a compound from Zingiber officinale (ginger), suppresses CETP and protects against atherosclerosis in twenty-four New Zealand male rabbits fed a normal or atherogenic diet, comparing it with atorvastatin over six weeks. 10-Dehydrogingerdione-treated rabbits showed a time-dependent, significant improvement in HDL cholesterol, correlated with the compound's ability to lower CETP. Lipoprotein(a), oxidised LDL, hsCRP, homocysteine, and MMP9 all decreased significantly with 10-dehydrogingerdione (P less than 0.001), performing similarly to atorvastatin on hsCRP and Lp(a), but better than atorvastatin on homocysteine, MMP9, and oxidised LDL. The authors conclude 10-dehydrogingerdione lowers LDL-C and raises HDL-C by suppressing CETP, identifying it as a potential natural CETP inhibitor for treating atherosclerosis and residual cardiovascular risk.
Original abstract
Objective: 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.
Methods: 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.
Results: 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).
Conclusions: 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.
Summary written by cetpinhibition.org from the published abstract; figures as published. Page updated 19 August 2026. Methods.