title: 10-Dehydrogingerdione raises HDL-cholesterol through a CETP inhibition and wards off oxidation and inflammation in dyslipidemic rabbits.
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.
authors.affiliation: Biochemistry Department, Faculty of Pharmacy, Zagazig University, Zagazig 44519, Egypt. Electronic address: mmelseweidy@yahoo.com.
authors.forename: Mohamed M
authors.initials: MM
authors.lastname: Elseweidy
authors.forename: Fatma R
authors.initials: FR
authors.lastname: Abdallah
authors.forename: Nahla N
authors.initials: NN
authors.lastname: Younis
authors.forename: Sameih
authors.initials: S
authors.lastname: Aldohmy
authors.forename: Haitham M
authors.initials: HM
authors.lastname: Kassem
mesh_terms: D000818:Animals; D000069059:Atorvastatin; D002097:C-Reactive Protein / Q000378:metabolism; D049109:Cell Proliferation; D053480:Cholesterol Ester Transfer Proteins / Q000037:antagonists & inhibitors / Q000502:physiology*; D008076:Cholesterol, HDL / Q000097:blood* / Q000378:metabolism; D004036:Diet, Atherogenic; D004195:Disease Models, Animal; D050171:Dyslipidemias / Q000097:blood*; D006139:Guaiacol / Q000031:analogs & derivatives* / Q000494:pharmacology; D006538:Heptanoic Acids / Q000494:pharmacology; D007249:Inflammation / Q000097:blood; D008297:Male; D013058:Mass Spectrometry; D010100:Oxygen / Q000378:metabolism*; D011758:Pyrroles / Q000494:pharmacology; D011817:Rabbits; D012307:Risk Factors
chemical_list: C561631:(10)-dehydrogingerdione; D053480:Cholesterol Ester Transfer Proteins; D008076:Cholesterol, HDL; D006538:Heptanoic Acids; D011758:Pyrroles; D006139:Guaiacol; D002097:C-Reactive Protein; D000069059:Atorvastatin; D010100:Oxygen
keywords: 10-Dehydrogingerdione; Atorvastatin; CETP inhibition; CRP; Dyslipidemia; HDL-C; Ox-LDL