Objective To observe the effects of turicamycin-inhibitor of N-glycosylation of proteins on expression of (?1 integrin,FAK and cyclin D1 in high glucose-induced glomerular mesangial cells (CMC), and to explore the mechanism concerned. Methods Cultured HBZY-1 rat mesangial cells were divided into 5 groups:control group;high glucose group;mannitol group;high glucose plus TM group; TM group.The expression of ?1 integrin was measured by flow cytometry, expression of FAK and cyclin D1 was measured by immunohistochemistry,and proliferation of GMCs was measured by MTT. Results There was a little expression of ?1 integrin, FAK and cyclin D1 on normal mesangial cells. High glucose induced the proliferation and increased the expression of ?1 integrin and cyclin D1.There was no significant difference in mannitol group as compared to control group.The expression of (?1 integrin FAK and cyclin D1 decreased notably by TM.TM could also decrease proliferative abilitiy of cells. All the effects of TM were dose-dependent. Conclusion Through blocking glycosylation of glycoprotein, TM can suppress cellular proliferation and expression of pi integrin induced by high glucose in a dose-dependent manners,then pi integrin affects the expression of FAK and cyclin D1.

AIM: To investigates the role of phosphatidic acid (PA) in the expression of several inflammatory mediators produced by glomerural macrophages (GM?). METHODS: The study was performed on a rat model of accelerated anti-glomerural basement membrane (anti-GBM) glomerulonephritis (GN). GN-GM? were isolated and identified. Peritoneal M? (P-M?) of both normal and GN rats were used as controls. Block and reverse test were investigated with rhIL-1? stimulated, lisofylline (LSF) and phosphatidic acid (PA). Macrophage expression of ICAM-1 and TGF-? 1 were assessed at the level of protein and gene by immunocytochemistry, northern blot and RT-PCR. RESULTS: (1) After stimulated with rhIL-1?, GN-GM? produced much more ICAM-1, MCP-1 and TGF-? 1 than P-M?, and it's gene expression was similar as protein product. (2) mRNA expression of these factors was up-regulated again after the GN-GM? were pretreated with LSF then PA was added. CONCLUSIONS: Since GN-GM? plays an important role for PA in the mediation of glomerular injury, inhibiting of PA production is the keypoint of blocking M? mediated inflammatory effects. LSF may be an effective medicine in therapy for acute inflammatory forms of GN.