ABSTRACT
The regulation mechanism of arecoline on rat hepatic CYP2E1 was studied in vivo. After oral administration of arecoline hydrobromide (AH; 4, 20 and 100 mg·kg-1·d-1) to rats for one week, the hepatic CYP2E1 mRNA level remained unchanged, but the hepatic CYP2E1 protein content was dose-dependently increased. Additionally, although the hepatic CYP2E1 activity was induced by AH treatment, the induction was attenuated with the increase in dosage. The results indicate that the effect of arecoline on rat hepatic CYP2El does not involve transcriptional activation of the gene, but largely involves the stabilization of CYP2E1 protein against degradation or increased efficiency of CYP2E1 mRNA translation, and additionally involve the post- translational modification of CYP2E1 protein. Furthermore, the CYP2E1 response is fairly equal among the different species, the induction of rat hepatic CYP2E1 by arecoline suggests that there is a risk of metabolic interaction among the substrate drugs of CYP2E1 in betel-quid use human.
ABSTRACT
The regulation mechanism of arecoline on rat hepatic CYP2E1 was studied in vivo. After oral administration of arecoline hydrobromide (AH; 4, 20 and 100 mg x kg(-1) x d(-1)) to rats for one week, the hepatic CYP2E1 mRNA level remained unchanged, but the hepatic CYP2E1 protein content was dose-dependently increased. Additionally, although the hepatic CYP2E1 activity was induced by AH treatment, the induction was attenuated with the increase in dosage. The results indicate that the effect of arecoline on rat hepaticdoes not involve transcriptional activation of the gene, but largely involves the stabilization of CYP2E1 protein against degradation or increased efficiency of CYP2E1 mRNA translation, and additionally involve the post- ranslational modification of CYP2E1 protein. Furthermore, the CYP2E1 response is fairly equal among the different species, the induction of rat hepatic CYP2E1 by arecoline suggests that there is a risk of metabolic interaction among the substrate drugs of CYP2E1 in betel-quid use human.
Subject(s)
Animals , Humans , Rats , Arecoline , Pharmacology , Cytochrome P-450 CYP2E1 , Metabolism , Cytochrome P-450 CYP2E1 Inducers , Pharmacology , Liver , Metabolism , RNA, MessengerABSTRACT
<p><b>OBJECTIVE</b>Ceramic brackets debonding by Nd:YAG laser is based on the thermal effect of laser, which may cause injury of the pulp tissue. In this study, the histological changes of pulp tissue that subjected to Nd: YAG laser irradiation with different power and time were observed.</p><p><b>METHODS</b>20 New Zealand rabbits were included in this study. Ceramic brackets were bonded to the 4 incisors as routine. The ceramic brackets of left upper teeth that debonded mechanically were used as control group, while the brackets of right upper, left lower and right lower incisors were debonded by laser with 3 W 3 s (group A), 2 W 5 s (group B) and 5 W 2 s (group C) energies, respectively. The teeth were pulled out at 5 minutes, 1 day, 3 days, 1 week and 1 month after the debonding operations. Slides prepared from the pulp tissues of the debonded teeth were used to evaluate the injury of laser.</p><p><b>RESULTS</b>In comparison with the control group, pulp tissue of teeth that exposed to laser with different energy for 5 minutes showed mild capillary dilation. One day later, group A, B and C showed moderate capillary dilation, and group C also showed moderate infiltration. At 3 days, inflammation was disappeared in group B, whereas capillary dilation was found in group A. Hemorrhage and inflammation cells infiltration were found in group C. At 1 week, alleviation of capillary dilation was found in group A but not in group C. One month later, inflammation disappeared in group A, while pulp tissue in group C showed mild edema and capillary dilation.</p><p><b>CONCLUSION</b>Nd:YAG laser of high energy may cause injury of the pulp tissue during debonding. Laser energy of 3 W 3 s could effectively debond ceramic brackets without irreversible pulp injury.</p>