Original Paper Pharmacology	Planta Med 2006; 72: 9-13 DOI: 10.1055/s-2005-916177
© Georg Thieme Verlag KG Stuttgart · New York
Mediation of β-Endorphin by Ginsenoside Rh2 to Lower Plasma Glucose in Streptozotocin-Induced Diabetic Rats
Dar-Ming Lai1, Yong-Kwang Tu1, I-Min Liu2, Pei-Feng Chen3, Juei-Tang Cheng3
1 Neurosurgical Division, Department of Surgery, National Taiwan University Hospital, Taipei City, Taiwan, R.O.C. 2 Department of Pharmacy, Tajen University, Yen-Pou, Ping Tung Shien, Taiwan, R.O.C. 3 Department of Pharmacology, College of Medicine, National Cheng Kung University, Tainan City, Taiwan, R.O.C.

Abstract

We investigated the plasma glucose-lowering mechanism(s) of Rh2, a ginsenoside derived from Panax ginseng, in rats with streptozotocin-induced diabetes (STZ-diabetic rats). After intravenous injection over 120 min into fasting STZ-diabetic rats, Rh2 decreased plasma glucose in a dose-dependent manner. In parallel to the lowering of plasma glucose, an increase of plasma β-endorphin-like immunoreactivity was observed. In addition, naloxone and naloxonazine at doses sufficient to block opioid μ-receptors inhibited the plasma glucose-lowering action of Rh2 in genetically wild-type, diabetic mice. In contrast, Rh2 failed to lower plasma glucose in opioid μ-receptor knockout diabetic mice. An increase in gene expression at both the mRNA and protein levels of glucose transporter subtype 4 (GLUT 4) was observed in soleus muscle obtained from STZ-diabetic rats treated with Rh2 three times daily for one day; this increase in expression was absent when opioid μ-receptors were blocked. In conclusion, our results suggest that ginsenoside Rh2 may lower plasma glucose in STZ-diabetic rats based on an increase in β-endorphin secretion that activates opioid μ-receptors thereby resulting in an increased expression of GLUT 4.

Key words

Ginsenoside Rh2 - streptozotocin-induced diabetic rats - β-endorphin - opioid μ-receptor