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J Ethnopharmacol. 2006 Mar 8;104(1-2):199-206. Epub 2005 Oct 3.
Mediation of beta-endorphin by myricetin to lower plasma glucose in streptozotocin-induced diabetic rats.
Liu IM, Liou SS, Cheng JT.
Department of Pharmacy, Tajen University, Yanpu Shiang, Ping Tung Shien, Taiwan, ROC.
Streptozotocin-induced diabetic (STZ-diabetic) rats were employed to investigate the mechanism(s) whereby myricetin, the active principle of Abelmoschus moschatus (Malvaceae), exerts its glucose-lowering effects. Myricetin was purified from the aerial portion of the plant and administered intravenously. A dose-dependent decrease in plasma glucose concentration was observed 30min following injection, in parallel with increased plasma beta-endorphin-like immunoreactivity (BER). Myricetin enhanced BER release similarly from isolated adrenal medulla. Plasma glucose-lowering and BER-elevating effects of myricetin were both eliminated after bilateral adrenalectomy. Myricetin failed to lower plasma glucose after treatment with opioid mu-receptor antagonists and in opioid mu-receptor knockout diabetic mice. Injection of myricetin three times daily for three consecutive days resulted in increased expression of the glucose transporter subtype 4 (GLUT 4) in soleus muscle and in reduced expression of phosphoenolpyruvate carboxykinase (PEPCK) in liver; these inductions were preventable by opioid mu-receptor blockade. Findings support the conclusion that the plasma glucose-lowering action of myricetin in insulin-deficient animals is mediated by activation of opioid mu-receptors of peripheral tissues in response to increased beta-endorphin secretion. Opioid mu-receptor activation is held responsible for the enhancement of muscle GLUT 4 gene expression and the attenuation of hepatic PEPCK gene expression observed in these myricetin-treated diabetic animals.
Planta Med. 2005 Jul;71(7):617-21.
Myricetin as the active principle of Abelmoschus moschatus to lower plasma glucose in streptozotocin-induced diabetic rats.
Liu IM, Liou SS, Lan TW, Hsu FL, Cheng JT.
Department of Pharmacy, Tajen Institute of Technology, Yen-Pou, Ping Tung Shien, Taiwan, R.O.C. firstname.lastname@example.org
The antihyperglycemic action of myricetin, purified from the aerial part of Abelmoschus moschatus (Malvaceae), was investigated in streptozotocin-induced diabetic rats (STZ-diabetic rats). Bolus intravenous injection of myricetin decreased the plasma glucose concentrations in a dose-dependent manner in STZ-diabetic rats. Myricetin at the effective dose (1.0 mg/kg) significantly attenuated the increase of plasma glucose induced by an intravenous glucose challenge test in normal rats. A stimulatory effect of myricetin on glucose uptake of the soleus muscles isolated from STZ-diabetic rats was obtained in a concentration-dependent manner from 0.01 to 10.0 micromol/L. The increase of glucose utilization by myricetin was further characterized using the enhancement of glycogen synthesis in isolated hepatocytes of STZ-diabetic rats. These results suggest that myricetin has an ability to enhance glucose utilization to lower plasma glucose in diabetic rats lacking insulin.
Braz J Med Biol Res. 2003 Dec;36(12):1613-20. Epub 2003 Nov 17.
Neuroprotection by flavonoids.
Dajas F, Rivera-Megret F, Blasina F, Arredondo F, Abin-Carriquiry JA, Costa G, Echeverry C, Lafon L, Heizen H, Ferreira M, Morquio A.
Departamento de Neuroquimica, Instituto de Investigaciones Biol gicas Clemente Estable, Universidade da Republica, Montevideo, Uruguay.
The high morbidity, high socioeconomic costs and lack of specific treatments are key factors that define the relevance of brain pathology for human health and the importance of research on neuronal protective agents. Epidemiological studies have shown beneficial effects of flavonoids on arteriosclerosis-related pathology in general and neurodegeneration in particular. Flavonoids can protect the brain by their ability to modulate intracellular signals promoting cellular survival. Quercetin and structurally related flavonoids (myricetin, fisetin, luteolin) showed a marked cytoprotective capacity in in vitro experimental conditions in models of predominantly apoptotic death such as that induced by medium concentrations (200 M) of H2O2 added to PC12 cells in culture. Nevertheless, quercetin did not protect substantia nigra neurons in vivo from an oxidative insult (6-hydroxydopamine), probably due to difficulties in crossing the blood-brain barrier. On the other hand, treatment of permanent focal ischemia with a lecithin/quercetin preparation decreased lesion volume, showing that preparations that help to cross the blood-brain barrier may be critical for the expression of the effects of flavonoids on the brain. The hypothesis is advanced that a group of quercetin-related flavonoids could become lead molecules for the development of neuroprotective compounds with multitarget anti-ischemic effects.
Gen Pharmacol. 1997 Aug;29(2):121-6.
Biological effects of myricetin.
Ong KC, Khoo HE.
Department of Biochemistry, Faculty of Medicine, National University of Singapore, Kent Ridge Crescent, Singapore.
1. Myricetin is a natural bioflavonoid whose occurrence in nature is widespread among plants. 2. It has been demonstrated to possess both antioxidative properties and prooxidative properties. 3. It is a potent anticarcinogen and antimutagen, although it has been shown to promote mutagenesis with the use of the Ames Test. 4. Its therapeutic potential and benefits in cardiovascular diseases and diabetes mellitus also are reviewed.