Antihyperglycemic action of andrographolide
碩士 === 國立成功大學 === 藥理學研究所 === 90 === In the present study, the antihyperglycemic action and possible mechanism of andrographolide were investigated. A dose-dependent lowering of plasma glucose was observed both in the streptozotocin (STZ)-induced diabetic rat and Wistar rats, after oral treatment (P....
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Format: | Others |
Language: | zh-TW |
Published: |
2002
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Online Access: | http://ndltd.ncl.edu.tw/handle/y5k76m |
Summary: | 碩士 === 國立成功大學 === 藥理學研究所 === 90 === In the present study, the antihyperglycemic action and possible mechanism of andrographolide were investigated. A dose-dependent lowering of plasma glucose was observed both in the streptozotocin (STZ)-induced diabetic rat and Wistar rats, after oral treatment (P.O.) of andrographolide. Andrographolide at an effective dose significantly attenuated the increase of plasma glucose induced by intravenous glucose challenge test in Wistar rats. Stimulatory effects of andrographolide on the glucose uptake and glycogen synthesis were also obtained in soleus muscles and hepatocytes isolated from STZ-diabetic rats indicating an increase of glucose utilization by androgrpholide in a way not dependent on insulin. In our previous study, we found that b-endorphin isresponsible for production of hypoglycemic effect is STZ-diabetic rats. Increase of plasma b-endorphin in STZ-diabetic rats seems important for compensation of hyperglycemia. Andrographolide at the effective dose increased the plasma b-endorphin level in STZ-diabetic rats. The plasma glucose lowering effect of andrographolide was also abolished by naloxone or naloxonazine. Plasma glucose lowering action of andrographolide at the dose effective in diabetic rats was disappeared in opioid m-receptors knockout mice. The obtained results suggest that the release of b-endorphin seems responsible for the lowering of plasma glucose in STZ-diabetic rats by andrographolide. Activation of opioid m-receptors by b-endorphin can increase the utilization of glucose and/or decrease hepatic gluconeogenesis to lower plasma glucose in diabetic rats lacking insulin.
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