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Original Paper

Effect of Bee Venom and Its Melittin on Apical Transporters of Renal Proximal Tubule Cells

Han H.J.a* · Lee J.H.b* · Park S.H.a · Choi H.J.a · Yang I.S.b · Mar W.C.c · Kang S.K.d · Lee H.J.d

Author affiliations

aDepartment of Veterinary Physiology, College of Veterinary Medicine, Hormone Research Center, Chonnam National University, Kwangju, bCollege of Veterinary Medicine and School of Agricultural Biotechnology, Seoul National University, Suwon, cNatural Products Research Institute, Seoul National University, Seoul, and dDepartment of Acupuncture and Moxibustion, College of Oriental Medicine, Kyung Hee University, Seoul, Korea

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Kidney Blood Press Res 2000;23:393–399

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Article / Publication Details

First-Page Preview
Abstract of Original Paper

Published online: November 02, 2000
Issue release date: 2000

Number of Print Pages: 7
Number of Figures: 4
Number of Tables: 3

ISSN: 1420-4096 (Print)
eISSN: 1423-0143 (Online)

For additional information: https://www.karger.com/KBR

Abstract

Renal failure by bee venom may be related to a malfunction of renal transporters. However, the effects of bee venom on apical membrane transporters of renal proximal tubular cells are not yet known. The aim of this study was to examine the effects of dried bee venom of Apis mellifera and its melittin on apical transporter activity of primary cultured rabbit kidney proximal tubule cells. Bee venom (1 μg/ml) decreased the cell viability and increased lactate dehydrogenase activity over 30–min treatments. Its effect was blocked by mepacrine or AACOCF3 (10–6 M; phospholipase A2 inhibitors). However, there was no effect on cell viability at a concentration of 0.01 μg/ml of bee venom. Thus, we investigated the effect of bee venom (1 μg/ml) on the activity of renal transporters at 30 min. Bee venom inhibited α–methyl–D–glucopyranoside, Pi, and Na+ uptakes, but increased Ca2+ uptake. These effects of bee venom were blocked by mepacrine or AACOCF3 (10–6 M), and bee venom–induced stimulation of Ca2+ uptake was also blocked by methoxyverapamil and nifedipine (L–type calcium channel blockers). In addition, bee venom increased [3H]–arachidonic acid release by 216 % of that of control. In all experiments, bee venom melittin (0.5 μg/ml) had an identical effect to that of bee venom itself. In conclusion, bee venom inhibited, in part, α–MG, Pi, and Na+ uptakes through its melittin which increased Ca2+ uptake and arachidonic acid release in primary cultured rabbit renal proximal tubule cells.


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Article / Publication Details

First-Page Preview
Abstract of Original Paper

Published online: November 02, 2000
Issue release date: 2000

Number of Print Pages: 7
Number of Figures: 4
Number of Tables: 3

ISSN: 1420-4096 (Print)
eISSN: 1423-0143 (Online)

For additional information: https://www.karger.com/KBR


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