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V infection group than in no infection group,while positive rate of other autoantibodies was not statistically different between the two groups.Conclusion Renal EBV infection may involve in the pathogenesis of LN by inducing the production of anti-Sm-Ab.
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Aim To investigate the effects of Panax Notoginsenosides(PNS) on the gene expression and protein excretion of TGF-?_1 and CTGF of human renal tubular epithelial cell induced by uremic serum in vitro.Methods Forty sera from CRF patients and twenty sera from healthy volunteers were collected,gently mixed,inactived and separated respectively in steriled condition.HK-2 Cells were cultured in RPMI-1640 medium with 10% newborn calves serum and subcultured routinely.They were differentiated by phase contrast microscope and scanning electron microscope detection and cytokeratin18(CK-18) immunohistochemistry method.The protein levels of TGF-?_1 were examined by enzyme-linked immunoadsordent assay(ELISA).The protein levels of CTGF were examined by Western Bloting assay.The gene expression of TGF-?_1 and CTGF was detected by Semi-quantitative reverse trainscriptase polymerase chain reaction(RT-PCR).Results TGF-?_1 and CTGF gene expression and protein level were increased in 10% uremic serum groups compared with that of normal control group(P
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Objective To investigate the effects of Free fatty acids (FFAs) on extracellular matrix(ECM) mRNA expression and secretion.Methods Rat glomerular mesangial cells(HBZY-1 cells) were cultured in vitro and stimulated with OA in different concentration.The expression of collagen Ⅳ(Col Ⅳ) and fibronectin (FN) and transforming growth factor-beta1(TGF-?_1) mRNA were measured by semi-quantitative RT-PCR.The levels of Col Ⅳ and FN in cultured supernatant were determined by ELISA.Results The mRNA expression of Col Ⅳ, FN and TGF-?_1 of 25、100、400 ?mol/L stimulated OA groups were 0.94?0.17、1.16?0.15、1.28?0.19 and 0.82?0.11、0.97?0.07、1.09?0.08 and 1.15? 0.07、1.24?0.06、1.36?0.05 respectively , which increased significantly compared with their control group(0.73?0.16、0.53?0.09、 0.96?0.11 P
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10 000 D uremic toxin through promoting the gene and protein expression of CTGF in renal tubular epithelial cells in patients with chronic renal failure.
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Objective:To study the effect of interleukin-18 on transdifferentiation in renal tubular epithelial cells(TECs).Methods:Human proximal tubular epithelial cell line(HK-2) was cultured in vitro.TECs were exposed to different concentrations(0,0.1,1,10 and 100 ng/ml) of IL-18 for 24,48 and 72 hours.At the end of each incubation,the expressions of the ?-SMA and TGF-?_1 mRNA were assessed by RT-PCR,the rate of ?-SMA expressing TECs was assessed by immunocytochemistry,and the expression of the ?-SMA protein was assessed by Western blotting.Results:(1)The expressions of ?-SMA and TGF-?_1 mRNA were increased significantly by a dose- and time-dependent manner when TECs were exposed to IL-18(P
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AIM: To investigate the effects of interleukin-13(IL-13) on the inflammatory reaction of glomerular mesangial cells. METHODS: TNF-? protein in the supernatant of cultured mesangial cells was determined with ELISA. ICAM-1 expression on the mesangial cells was determined with flow cytometry. The expression of TNF-? mRNA and ICAM-1 mRNA were semiquantatively tested with RT-PCR. RESULTS: Mesangial cells did not constitutively express TNF-? mRNA and TNF-? protein. Induced by LPS(10 mg/L) for 24 h, mesangial cells expressed TNF-? mRNA and TNF-? protein at a high level. At the concentration of 1 ?g/L and 10?g/L, IL-13 markedly inhibited LPS-induced TNF-? mRNA and protein expression in mesangial cells. At the concentration of 100?g/L, IL-13 completely inhibited LPS-induced TNF-? mRNA and protein expression in mesangial cells. ICAM-1 constitutively expressed on the surface of mesangial cells at very low level. Induced by TNF-?(100?g/L), mesangial cells expressed ICAM-1 mRNA and ICAM-1 cell surface molecule at high level. Costimulated mesangial cells with IL-13(10?g/L) and TNF-?(100?g/L), IL-13 inhibited TNF-?-induced ICAM-1 mRNA and cell surface molecule expression at every time course. CONCLUSION: IL-13 not only inhibits LPS-induced TNF-? expression but also inhibits TNF-?-induced ICAM-1 expression in mesangial cells. These data suggest that IL-13 inhibits the inflammatory reaction in mesangial cells.
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AIM: To investigate the effect of cyclophosphamide(CTX) on proliferation and apoptosis of mesangial cells(GMC) of rat in vitro. METHODS: GMC proliferation was detected by MTT method, GMC apoptosis was examined by inverted microscopy for phase-contract and fluoroscopy and flow cytometry analysis. The levels of Fas and Bcl-2 were also detected by immunohistology. RESULTS: The proliferation of GMC were inhibited by CTX, methylprednisolone(MP), low molecular weight heparin(LMWH). Apoptosis of GMC was induced by CTX, the apoptosis rate of GMC was 8.2%, and the Fas level was increased. CONCLUSION: CTX could inhibit proliferation and induce apoptosis of GMC possibly by enhancing the Fas level.