Ja-Ping Shieh

Publications (2)4.61 Total impact

• Article: Plasma glucose lowering mechanisms of catalpol, an active principle from roots of Rehmannia glutinosa, in streptozotocin-induced diabetic rats.

  Ja-Ping Shieh, Kai-Chun Cheng, Hsien-Hui Chung, Ya-Fan Kerh, Ching-Hua Yeh, Juei-Tang Cheng
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  ABSTRACT: Catalpol is one of the active principles from roots of Rehmannia glutinosa Steud (Scrophulariaceae) that is widely used to treat diabetic disorders in Chinese traditional medicine using the name of Di-Huang, which is used to investigate the mechanisms for lowering of plasma glucose in streptozotocin-induced diabetic rats (STZ-diabetic rats). Catalpol decreased plasma glucose in a dose-related manner, and this action was reduced by pretreatment with naloxone or naloxonazine. An increase of plasma β-endorphin by catalpol was also observed in parallel. The plasma glucose lowering action of catalpol was deleted in bilateral adrenalectomized rats. Moreover, catalpol enhanced β-endorphin release from the isolated adrenal medulla of STZ-diabetic rats. Otherwise, plasma glucose lowering action of catalpol failed to produce in opioid μ-receptor knockout mice. Also, repeated administration of catalpol for 3 days in STZ-diabetic rats resulted in a marked reduction of phosphoenolpyruvate carboxykinase (PEPCK) expression in liver and an increased expression of glucose transporter subtype 4 (GLUT 4) in skeletal muscle. These effects were also reversed by blockade of opioid μ-receptors. Our results suggested that catalpol increased glucose utilization through increase of β-endorphin secretion from adrenal gland in STZ-diabetic rats.
  Journal of Agricultural and Food Chemistry 03/2011; 59(8):3747-53. · 2.82 Impact Factor
• Article: Activation of peripheral opioid µ-receptors in blood vessel may lower blood pressure in spontaneously hypertensive rats.

  Zhih-Cherng Chen, Ja-Ping Shieh, Hsien-Hui Chung, Ching-Hsia Hung, Hung Jung Lin, Juei-Tang Cheng
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  ABSTRACT: The role of opioid receptors in the regulation of vascular function remains unclear. In the current study, we evaluated the ability of loperamide, a peripheral opioid receptor agonist, to regulate blood pressure in spontaneously hypertensive rats (SHRs) and examined the mechanism(s) by which loperamide exerts its effects. In male SHRs, mean arterial pressure (MAP) was measured and hemodynamic analysis was recorded. Additionally, the isometric tension of aortic rings isolated from SHRs was determined. Loperamide dose-dependently decreased MAP in SHRs but not in the normal group of Wistar-Kyoto rats. This reduction of MAP in conscious SHRs was abolished by the selective opioid μ-receptor antagonist cyprodime, but not by naloxonazine, the μ(1)-opioid receptor antagonist. However, cardiac output was not altered by loperamide in anesthetized SHRs. Moreover, loperamide-induced relaxation in isolated aortic rings precontracted with phenylephrine or vasopressin. This relaxation was abolished by cyprodime, but not by naloxonazine. Loperamide-induced relaxation was also attenuated by glibenclamide, an ATP-sensitive potassium (K(ATP)) channel blocker. Additionally, vasodilatation by loperamide was reduced by an inhibitor of protein kinase A (PKA) and enhanced by an inhibitor of phosphodiesterases. We suggest that loperamide can lower MAP in SHRs via μ(2)-opioid receptor-dependent cAMP-PKA pathway that induces vascular relaxation by opening K(ATP) channels.
  Pharmacology 01/2011; 87(5-6):257-64. · 1.79 Impact Factor