RÉSUMÉ
Objective To establish detection method of glinides adulterated illegally in hypoglycemic traditional Chinese medi -cine (TCM) by surface enhanced Raman spectroscopy (SERS).Methods Adulterated chemicals and TCM matrixes were separated by TLC first.Then trace substances in TLC plate was tested by SERS method .By investigating SERS detection conditions of glinides chemi-cals in simulated positive samples , a detection method was established to detect illegal adulterant in hypoglycemic TCM .Results Better SERS spectra of glinides could be obtained by silver sol prepared with organic solvent DMF .Conclusion The detection method coupled with TLC and SERS in this paper was simple , fast and economical which could be used to detect glinides adulterated illegally in hypogly -cemic Chinese patent medicine quickly .
RÉSUMÉ
We have recently demonstrated that some anti-diabetic drugs such as biguanide and thizolidinediones administered centrally modulate the blood glucose level, suggesting that orally administered anti-diabetic drugs may modulate the blood glucose level by acting on central nervous system. The present study was designed to explore the possible action of another class of anti-diabetic drugs, glinidies, administered centrally on the blood glucose level in ICR mice. Mice were administered intracerebroventricularly (i.c.v.) or intrathecally (i.t.) with 5 to 30 microg of repaglinide or nateglinide in D-glucose-fed and streptozotocin (STZ)-treated models. We found that i.c.v. or i.t. injection with repaglinide dose-dependently attenuated the blood glucose level in D-glucose-fed model, whereas i.c.v. or i.t. injection with nateglinide showed no modulatory action on the blood glucose level in D-glucose-fed model. Furthermore, the effect of repaglinide administered i.c.v. or i.t. on the blood glucose level in STZ-treated model was studied. We found that repaglinide administered i.c.v. slightly enhanced the blood glucose level in STZ-treated model. On the other hand, i.t. injection with repaglinide attenuated the blood glucose level in STZ-treated model. The plasma insulin level was enhanced by repaglinide in D-glucose-fed model, but repaglinide did not affect the plasma insulin level in STZ-treated model. In addition, nateglinide did not alter the plasma insulin level in both D-glucose-fed and STZ-treated models. These results suggest that the anti-diabetic action of repaglinide appears to be, at least, mediated via the brain and the spinal cord as revealed in both D-glucose fed and STZ-treated models.