Anti-Diabetic Effects of Madecassic Acid and Rotundic Acid

Nutrients. 2015 Dec 2;7(12):10065-75. doi: 10.3390/nu7125512.

Abstract

Anti-diabetic effects of madecassic acid (MEA) and rotundic acid (RA) were examined. MEA or RA at 0.05% or 0.1% was supplied to diabetic mice for six weeks. The intake of MEA, not RA, dose-dependently lowered plasma glucose level and increased plasma insulin level. MEA, not RA, intake dose-dependently reduced plasminogen activator inhibitor-1 activity and fibrinogen level; as well as restored antithrombin-III and protein C activities in plasma of diabetic mice. MEA or RA intake decreased triglyceride and cholesterol levels in plasma and liver. Histological data agreed that MEA or RA intake lowered hepatic lipid droplets, determined by ORO stain. MEA intake dose-dependently declined reactive oxygen species (ROS) and oxidized glutathione levels, increased glutathione content and maintained the activity of glutathione reductase and catalase in the heart and kidneys of diabetic mice. MEA intake dose-dependently reduced interleukin (IL)-1β, IL-6, tumor necrosis factor-α and monocyte chemoattractant protein-1 levels in the heart and kidneys of diabetic mice. RA intake at 0.1% declined cardiac and renal levels of these inflammatory factors. These data indicated that MEA improved glycemic control and hemostatic imbalance, lowered lipid accumulation, and attenuated oxidative and inflammatory stress in diabetic mice. Thus, madecassic acid could be considered as an anti-diabetic agent.

Keywords: anti-lipid; coagulation; diabetes; madecassic acid; rotundic acid.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Antithrombin III / genetics
  • Antithrombin III / metabolism
  • Blood Glucose / metabolism
  • Chemokine CCL2 / metabolism
  • Cholesterol / blood
  • Diabetes Mellitus, Experimental / drug therapy*
  • Dose-Response Relationship, Drug
  • Fibrinogen / genetics
  • Fibrinogen / metabolism
  • Glutathione / metabolism
  • Glutathione Reductase / metabolism
  • Hypoglycemic Agents / pharmacology*
  • Insulin / blood
  • Interleukin-1beta / metabolism
  • Interleukin-6 / metabolism
  • Kidney / drug effects
  • Kidney / metabolism
  • Liver / drug effects
  • Liver / metabolism
  • Male
  • Mice
  • Mice, Inbred BALB C
  • Plasminogen Activator Inhibitor 1 / genetics
  • Plasminogen Activator Inhibitor 1 / metabolism
  • Reactive Oxygen Species / metabolism
  • Triglycerides / blood
  • Triterpenes / pharmacology*
  • Tumor Necrosis Factor-alpha / metabolism

Substances

  • Blood Glucose
  • Ccl2 protein, mouse
  • Chemokine CCL2
  • Hypoglycemic Agents
  • Insulin
  • Interleukin-1beta
  • Interleukin-6
  • Plasminogen Activator Inhibitor 1
  • Reactive Oxygen Species
  • Triglycerides
  • Triterpenes
  • Tumor Necrosis Factor-alpha
  • rotundic acid
  • Antithrombin III
  • Fibrinogen
  • Cholesterol
  • Glutathione Reductase
  • Glutathione
  • madecassic acid