Pharmacognosy Lecture Notes 45.pdf
Pharmacognosy Lecture Notes 45.pdf
Pharmacognosy Lecture Notes 45.pdf
products 45. 7. Synergy and other interactions in phytomedicine 53. Williamson E.M. 8. Traditional medicinal plants as a source of new drugs 62. 7. Synergy and other interactions in phytomedicine 53. Williamson E. M. 8. Traditional medicinal plants as a source of new drugs 42. 7. Synergy and other interactions in phytomedicine 53. Williamson E.M. 8. Traditional medicinal plants as a source of new drugs 42. 7. Synergy and other interactions in phytomedicine 53. Williamson EM 8. Traditional medicinal plants as a source of new medicines 42. 7. Synergy and other interactions in phytomedicine 53. Williamson E.
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/np.php?p=14950&type=1&tp=2. home page Pharmacy. SE EP TH CL M W O R. Pharmacognosy lecture notes and study guides.. Drug Distribution. Pharmacy Lecture Notes 45.pdf.. 1882.
/content/lng/pdf/hospital/volume/17/17-3/abc-fs-pharmacognosy.pdf. pharmacognosy lecture notes.
LEARN-TAKE ALL THE. BOOKS SOURCE PHARMACOGNOSY. CLASS. LECTURE. NOTES.. GEORGETOWN UNIVERSITY. What Is Pharmacognosy? What Is Pharmacognosy?.Cytotoxicity of benzoic acid related to glucose metabolism.
Benzoic acid (BA) is a naturally occurring plant product and widely used chemical, which is known to induce glucose metabolism disorder in animals. In the present study, we investigated effects of BA on human cell growth and glucose metabolism in relation to different molecular mechanisms. BA suppressed the growth of human normal fibroblast MRC-5 cells as well as human cancerous KB and KB-VIN cells. The antiproliferative activities of BA were abolished by actinomycin D and cycloheximide but not by 5,5-dimethyl-1-pyrolline-N-oxide and sodium azide, suggesting the involvement of both de novo protein synthesis and protein formation. In addition, BA induced expression of the glucose transporter GLUT4 at the mRNA and protein levels but markedly inhibited the activities of hexokinase (HK), and pyruvate kinase (PK). Transfection of human GLUT4 complementary DNA in human KB cells significantly prevented the growth inhibition and inhibition of HK and PK activities caused by BA. Among various serine/threonine protein kinases, cyclin-dependent protein kinase-2 (Cdk-2), which regulates the cell cycle, was significantly activated by BA and exhibited dose-dependent increase. In normal and cancerous KB and KB-VIN cells, BA markedly increased activity and expression of Cdk-2 whereas benzyl isonicotinic acid (BIA), an inactive analog of BA, failed to do so. Inhibition of Cdk-2 activity by Roscovitine, a specific inhibitor, significantly blocked BA-induced growth inhibition, GLUT4 expression, HK activity, and PK activity.
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