Biomedical subjects
Publications and source records attributed to H J Koh.
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Ginsenosides are involved in protective action against renal dysfunction and the regulation of renal functions. However, the effects of ginsenosides on glucose reabsorption are not yet known in renal proximal tubular cells. The aim of this study was to examine the effects of ginsenosides, protopanaxadiol (PD) saponin and protopanaxatriol (PT) saponin, on alpha-methyl-D-glucopyranoside (alpha-MG) uptake and its mechanism of action in primary cultured rabbit renal proximal tubular cells (PTCs). The alpha-MG uptake was inhibited by 90% by 0.5mM phloridizin and by removal of Na+ in the PTCs. These are typical characteristics described for the proximal tubule. To determine the time- and dose-dependent effects of PD and PT saponins on alpha-MG uptake, PTCs were incubated with different concentrations of PD and PT saponins (10-100 microg/ml) and for different time periods (from 10 min to 24 h). PT saponin (>/=50 microg/ml) from 30 min inhibited alpha-MG uptake; however, PD saponin did not alter the alpha-MG uptake at any doses and time periods. In the kinetic analysis of alpha-MG uptake, PT saponin produced a significant decrease in Vmax. The PT saponin induced inhibition of alpha-MG uptake was blocked by mepacrine, a phospholipase A2 inhibitor. In addition, PT saponin increased [3H] arachidonic acid release by 218% of that of control, and this effect was also completely blocked by mepacrine. In conclusion, PT saponin inhibited, in part, alpha-MG uptake through the phospholipase A2 signal pathway in primary cultured rabbit renal PTCs.
The aim of the present study was to examine the signaling pathways for a low dose of angiotensin II (ANG II) on Na+ uptake of primary cultured rabbit renal proximal tubule cells (PTCs) in hormonally defined serum-free medium. The results were as follows; ANG II (10(-11) M) stimulated the proliferation of PTCs. 10(-11) M ANG II stimulated Na+ uptake by 20%, whereas 10(-9) M ANG II inhibited it by 20% (p < 0.05). The stimulatory effect of 10(-11) M ANG II on Na+ uptake was inhibited by amiloride (10(-3) M) and by losartan (ANG II receptor subtype 1 antagonist, 10(-8) M) but not by PD123319 (ANG II receptor subtype 2 antagonist, 10(-8) M). Pertussis toxin (PTX, 50 ng/ml) prevented the ANG II-induced stimulation of Na+ uptake (p < 0.01). 8-Bromoadenosine 3', 5'-cyclic monophosphate (8-Br-cAMP, 10(-6) M) did not affect Na+ uptake. SQ 22536 (adenylate cyclase inhibitor, 10(-6) M) also did not change the ANG II-induced stimulation of Na+ uptake. ANG II did not stimulate cAMP production. In contrast, 12-O-tetradecanoylphorbol-13-acetate (TPA, 0.01 ng/ml) produced significant increase in Na+ uptake. When ANG II and TPA were added together to the PTCs, there was no additive effect on Na+ uptake. Staurosporine (calcium-dependant protein kinase C inhibitor, 10(-6) M) led to a complete inhibition of ANG II-induced stimulation of Na+ uptake. ANG II-treatment resulted in a 26% increase in total protein kinase C (PKC) activity. However, 10(-11) M ANG II did not change [Ca2+]i mobilization and [3H]-AA release while 10(-9) M ANG II increased both of them. In conclusion, the PTX-sensitive PKC pathway may be the main signaling cascade in the stimulatory effects of low dose of ANG II (10(-11) M) on Na+ uptake in the primary cultured rabbit renal proximal tubule cells in hormonally defined serum-free medium.
Polyphosphazenes possess polymer backbones consisting of nitrogen and phosphorous formally separated by alternating single and double bonds. Their potential for biomedical applications stems from the fact that polymers with a wide array of properties can be synthesized using the same starting compound, poly(dichlorophosphazene), through changes in side chain substituents, and that many of these compounds synthesized have been found to biodegrade to harmless products. In this article, studies of a novel monolithic bioerodible polyphosphazene matrix system for controlled drug delivery are presented. Poly(imidazole methylphenoxy)phosphazene is synthesized and shown to be bioerodible. The versatility of drug delivery devices fabricated using this polymer is shown through studies of release of macro-molecules and low molecular weight drugs. Initial histological evaluations of this particular polyphosphazene are also presented.