Résumé
Objective: To study the various processes involved in transcellular transport (TT) of huperzine A alone or in combination with ginkgolide B in Caco-2 and Madin-Darby canine renal (MDCK) cell monolayer. Methods: The transepithelial passage was assayed in the apical-to-basolateral (AP to BL) direction and opposite direction (BL to AP) in both cell lines. The determination of huperzine A and ginkgolide B were performed by high performance liquid chromatography (HPLC). The passage rates of huperzine A and ginkgolide B were calculated. Bi-directional TT (absorption and secretion) were taken in huperzine A and ginkgolide B in Caco-2 and MDCK cell monolayer. Results: TT absorption and secretion kinetics of huperzine A and ginkgolide B across two cells existed at the same time. The passage rates of huperzine A were increased significantly with adding different concentrations of ginkgolide B. Conclusions: The compound preparations of HA in combination with GB for dementia caused by cerebral ischemic have synergistic effects on the pharmacodynamics, and improve the bioavailability through BBB.
Résumé
OBJECTIVE@#To study the various processes involved in transcellular transport (TT) of huperzine A alone or in combination with ginkgolide B in Caco-2 and Madin-Darby canine renal (MDCK) cell monolayer.@*METHODS@#The transepithelial passage was assayed in the apical-to-basolateral (AP to BL) direction and opposite direction (BL to AP) in both cell lines. The determination of huperzine A and ginkgolide B were performed by high performance liquid chromatography (HPLC). The passage rates of huperzine A and ginkgolide B were calculated. Bi-directional TT (absorption and secretion) were taken in huperzine A and ginkgolide B in Caco-2 and MDCK cell monolayer.@*RESULTS@#TT absorption and secretion kinetics of huperzine A and ginkgolide B across two cells existed at the same time. The passage rates of huperzine A were increased significantly with adding different concentrations of ginkgolide B.@*CONCLUSIONS@#The compound preparations of HA in combination with GB for dementia caused by cerebral ischemic have synergistic effects on the pharmacodynamics, and improve the bioavailability through BBB.
Résumé
Magnesium is the second most common intracellular divalent cation. Magnesium balance in the body is controlled by a dynamic interplay among intestinal absorption, exchange with bone, and renal excretion. Intestinal magnesium absorption proceeds in both a passive paracellular and an active transcellular manner. Regulation of serum magnesium concentrations is achieved mainly by control of renal magnesium reabsorption. Only 20% of filtered magnesium is reabsorbed in the proximal tubule, whereas 60% is reclaimed in the cortical thick ascending limb (TAL) and another 5-10% in the distal convoluted tubule (DCT). The passive paracellular transport of magnesium in the TAL is closely related with the mutations in claudin-16/paracellin-1 and is responsible for familial hypomagnesemia with hypercalciuria and nephrocalcinosis. The active transcellular transport of magnesium in the DCT was similarly enhanced by the realization that defects in transient receptor potential melastatin 6 (TRPM6) cause hypomagnesemia with secondary hypocalcemia. This channel regulates the apical entry of magnesium into epithelia and alters whole-body magnesium homeostasis by controlling urinary excretion. TRPM6 is regulated at the transcriptional level by acid-base status, 17beta-estradiol, and both FK506 and cyclosporine. The molecular identity of the protein responsible for the basolateral exit of magnesium from the epithelial cell remains unidentified.