The beneficial effects of morroniside on the inflammatory response and lipid metabolism in the liver of db/db mice.
The effect of morroniside on lipid metabolism and the inflammatory response in the liver of type 2 diabetes model mice was investigated in this study. Male C57BLKS/J db/db mice were divided into the three groups: control (vehicle), morroniside 20, or 100 mg/kg body weight-treated mice. The elevated serum triglyceride and alanine aminotransferase levels as well as hepatic glucose and lipids contents in db/db mice were significantly decreased by the 8-week oral administration of morroniside in a dose-dependent manner. The generations of hepatic thiobarbituric acid-reactive substances and reactive oxygen species induced by hyperglycemia and dyslipidemia were also significantly decreased by the administration of morroniside. In addition, the barometer of an antioxidative state, the oxidized to reduced glutathione ratio, in the liver of db/db mice was markedly increased by morroniside treatment. From protein analysis, the elevated expressions of nuclear factor-kappaBp65, cyclooxygenase-2, inducible nitric oxide synthase, and sterol regulatory element binding proteins (SREBP-1 and SREBP-2) were down-regulated in the liver of db/db mice. On the other hand, the administration of morroniside significantly increased hepatic peroxisome proliferator activated receptor alpha expression. These results suggest that morroniside would act as a regulator of hepatic inflammatory reactions and lipid metabolism in db/db mice.
Park
Chan Hum
CH
Institute of Natural Medicine, University of Toyama, Sugitani, Toyama 930-0194, Japan.
Yamabe
Noriko
N
Noh
Jeong Sook
JS
Kang
Ki Sung
KS
Tanaka
Takashi
T
Yokozawa
Takako
T
D000410:Alanine Transaminase / Q000097:blood; D000818:Animals; D000893:Anti-Inflammatory Agents / Q000494:pharmacology / Q000627:therapeutic use*; D000975:Antioxidants / Q000494:pharmacology / Q000627:therapeutic use; D029768:Cornus / Q000737:chemistry*; D003921:Diabetes Mellitus, Experimental / Q000188:drug therapy* / Q000378:metabolism; D015536:Down-Regulation; D005638:Fruit; D015870:Gene Expression; D005947:Glucose / Q000378:metabolism; D005978:Glutathione / Q000378:metabolism; D006027:Glycosides / Q000494:pharmacology / Q000627:therapeutic use*; D000960:Hypolipidemic Agents / Q000494:pharmacology / Q000627:therapeutic use*; D018836:Inflammation Mediators / Q000097:blood; D050356:Lipid Metabolism / Q000187:drug effects; D008099:Liver / Q000187:drug effects* / Q000378:metabolism; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D018345:Mice, Knockout; D047493:PPAR alpha / Q000378:metabolism; D008517:Phytotherapy; D010936:Plant Extracts / Q000494:pharmacology / Q000627:therapeutic use*; D017382:Reactive Oxygen Species / Q000378:metabolism; D051780:Sterol Regulatory Element Binding Protein 1 / Q000378:metabolism; D051782:Sterol Regulatory Element Binding Protein 2 / Q000378:metabolism; D013858:Thiobarbiturates / Q000378:metabolism; D014280:Triglycerides / Q000097:blood
D000893:Anti-Inflammatory Agents; D000975:Antioxidants; D006027:Glycosides; D000960:Hypolipidemic Agents; D018836:Inflammation Mediators; D047493:PPAR alpha; D010936:Plant Extracts; D017382:Reactive Oxygen Species; C497388:Srebf1 protein, mouse; C497391:Srebf2 protein, mouse; D051780:Sterol Regulatory Element Binding Protein 1; D051782:Sterol Regulatory Element Binding Protein 2; D013858:Thiobarbiturates; D014280:Triglycerides; C488401:morroniside; D000410:Alanine Transaminase; D005978:Glutathione; D005947:Glucose; C029684:thiobarbituric acid