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Prednisolone‐loaded liposome decreases the accumulation of glomerular extracellular matrix and glomerular injury of immunoglobulin A nephropathy in ddY mice
Author(s) -
LIAO Jie,
HAYASHI Kayo,
HORIKOSHI Satoshi,
USHIJIMA Hideto,
KIMURA Junji,
TOMINO Yasuhiko
Publication year - 2002
Publication title -
nephrology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.752
H-Index - 61
eISSN - 1440-1797
pISSN - 1320-5358
DOI - 10.1046/j.1440-1797.2002.00099.x
Subject(s) - psl , prednisolone , extracellular matrix , glomerulonephritis , liposome , medicine , saline , nephropathy , endocrinology , microbiology and biotechnology , kidney , chemistry , biology , biochemistry , geometry , mathematics , diabetes mellitus
SUMMARY: Morphometric, immunofluorescent and electron microscopic analyses were performed to determine the glomerular changes of ddY mice after treatment with the prednisolone‐loaded liposome (PSL‐liposome) in the present study. A morphometric analysis including the extracellular matrix areas (ECMA), number of intraglomerular cell nuclei (NIGCN), and the ratio of glomerular tuft area (GTA) to the whole glomerular area (WGA) (GTA/WGA), or the ratio of glomerular Bowman's space (GBS) to GTA (GBS/GTA) was performed by image analysis using light microscopy. Extracellular matrix case, NIGCN and GTA/WGA of PSL‐liposome‐treated ddY mice were significantly decreased compared with those of ordinary prednisolone (PSL)‐treated and saline control ddY mice. Glomerular Bowman's space/GTA was markedly increased in the PSL‐liposome‐treated ddY mice. the mean intensity of immunoglobulin (Ig)A, IgG, complement C3 or intercellular adhesion molecule‐1 (ICAM‐1) staining in glomeruli of the PSL‐liposome treated ddY mice was also significantly decreased compared with those of ordinary PSL‐treated and saline control ddY mice. Electron dense deposits in glomeruli were decreased after treatment with PSL‐liposome in 61‐week‐old ddY mice. It appears that PSL‐liposome therapy might reduce glomerular expansion, and intraglomerular cell proliferation and infiltration in IgA nephropathy of ddY mice.