Effect of saikosaponin-d on rat's glomerular mesangial cell proliferation and extracellular matrix hyperplasia in vitro.
- Author:
Ning ZU
1
;
Xi DONG
;
Gui-xiang FU
Author Information
- Publication Type:Journal Article
- MeSH: Animals; Apoptosis; drug effects; Cell Cycle; drug effects; Cell Proliferation; drug effects; Cell Survival; drug effects; Cells, Cultured; Collagen Type IV; analysis; Cyclin-Dependent Kinase 4; metabolism; Enzyme-Linked Immunosorbent Assay; Extracellular Matrix; drug effects; pathology; Flow Cytometry; Hyperplasia; Immunohistochemistry; Immunosuppressive Agents; pharmacology; Lipopolysaccharides; Male; Mesangial Cells; cytology; drug effects; metabolism; Oleanolic Acid; analogs & derivatives; pharmacology; Rats; Rats, Sprague-Dawley; Saponins; pharmacology; Transforming Growth Factor beta1; analysis
- From: Chinese Journal of Integrated Traditional and Western Medicine 2007;27(4):321-325
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo investigate the effects of saikosaponin-d (SSd) on glomerular mesangial cells (MCs) proliferation and hyperplastic extracellular matrix (ECM) induced by lipopolysaccharide (LPS) to provide experimental proof for its use in prevention and treatment of glomerulosclerosis.
METHODSRat's MCs were cultivated and identified. The cultured MCs were stimulated by LPS and incubated with different concentrations of SSd. Cell proliferation was determined by MTT assay, LDH assay and flow cytometry, respectively. Type IV collagen (Col IV), fibronectin (FN) and transforming growth factor beta1 (TGF-beta1) in the conditioned medium were measured by ELISA. The expressions of cyclin-dependent kinase 4 (CDK4), c-Jun and c-Fos were detected by immunohistochemistry.
RESULTSAfter treated by SSd, MC proliferation was inhibited, cells in G0/G1 phase increased, and apoptosis induced. Moreover, secretion of Col IV, FN and TGF-beta1 and the expressions of CDK4, c-Jun and c-Fos in MC were inhibited.
CONCLUSIONThe inhibitory action of SSd on glomerulosclerosis was realized through inhibiting the expressions of CDK4, c-J un and c-Fos.
