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      Dilazep Hydrochloride, an Antiplatelet Drug, Inhibits Lipopolysaccharide-Induced Mouse Mesangial Cell IL-6 Secretion and Proliferation

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          Background: Antiplatelet agents have been widely used to reduce proteinuria and to prevent the progression of chronic glomerulonephritis or diabetic nephropathy to end-stage renal failure. Dipyridamole, one type of antiplatelet drug, inhibits the proliferation of glomerular mesangial cells (MCs). The effect of dilazep hydrochloride (dilazep) on these cells is still obscure. The effects of dilazep on cultured MC IL-6 secretion and proliferation were investigated in the present study. Methods: IL-6 secretion from MC induced by bacterial lipopolysaccharide (LPS) were assessed using sandwich ELISA. LPS-induced MC proliferation was detected by <sup>3</sup>H-thymidine incorporation and WST-1 assay (similar to MTT assay). Results: Incubation of MCs with various dosages of LPS (0, 1, 10, 50 and 100 ng/ml) induced IL-6 secretion in a dose-dependent manner. However, dilazep significantly inhibited this LPS-induced IL-6 secretion from MCs in a dose- and time-dependent manner. Dilazep also significantly inhibited MC proliferation in a dose-dependent manner. Conclusion: It appears that these effects of dilazep may prevent progression of mesangial proliferative glomerulonephritis.

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          Dipyridamole Inhibits Human Mesangial Cell Proliferation

          Background: Many glomerular diseases are associated with mesangial cell proliferation and the accumulation of extracellular matrix. At present, there are, however, few treatments which can inhibit these processes. The current study assessed the effects of the anti-platelet and putative anti-proliferative drug dipyridamole (DP) on the growth of human mesangial cells in vitro and their production of the extracellular matrix protein, fibronectin. Methods: Human mesangial cell proliferation, both intrinsic and stimulated by platelet-derived growth factor, was assessed using 3 H-thymidine incorporation and an MTT proliferation assay. A sandwich enzyme-linked immunosorbent assay was used to study the effects of DP on fibronectin synthesis, again in cells stimulated by transforming growth factor beta 1 and in unstimulated cells. Results: At concentrations compatible with the serum levels found in subjects consuming standard dosages, DP significantly inhibited the growth of human mesangial cells in vitro in a dose-dependent fashion. DP also abrogated the mitogenic effects of platelet-derived growth factor. It had no significant effects on the synthesis of fibronectin by these cells (either spontaneous or induced by transforming growth factor beta 1). There was no evidence of cytotoxicity. Conclusion: These data suggest that DP may have a therapeutic role in proliferative glomerulonephritis and possibly other diseases characterized by cell proliferation.

            Author and article information

            Kidney Blood Press Res
            Kidney and Blood Pressure Research
            S. Karger AG
            24 January 2001
            : 24
            : 1
            : 33-38
            Division of Nephrology, Department of Medicine, Juntendo University School of Medicine, Tokyo, Japan
            54203 Kidney Blood Press Res 2001;24:33–38
            © 2001 S. Karger AG, Basel

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            Page count
            Figures: 6, References: 19, Pages: 6
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            Original Paper

            Cardiovascular Medicine, Nephrology

            Mesangial cell proliferation, Interleukin-6, Dilazep


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