Influence and analysis of low-dosage steroid therapy in severe aristolochic acid nephropathy patients.

Aim: To investigate the effect of low-dosage steroid therapy in patients with severe aristolochic acid nephropathy (AAN).

Methods: Forty-three chronic AAN patients in the Peking Union Medical College Hospital and the First Affiliated Hospital of Xinxiang Medical College were included in this study from November 1998 to October 2013. According to the treatment method, the patients were divided into a steroid group (SG, n = 25) and a control group (CG, n = 18).

VEGF suppresses epithelial-mesenchymal transition by inhibiting the expression of Smad3 and miR‑192, a Smad3-dependent microRNA.

Transforming growth factor-β1 (TGF-β1)‑induced epithelial‑mesenchymal transition (EMT) is one of the important cellular and molecular mechanisms involved in renal fibrosis. Smad3 and miR-192 (a Smad3-dependent microRNA) are involved in TGF-β1-mediated EMT. Vascular endothelial growth factor (VEGF) is a renal tubular epithelial survival factor.

VEGF ameliorates tubulointerstitial fibrosis in unilateral ureteral obstruction mice via inhibition of epithelial-mesenchymal transition.

Aim: Vascular endothelial growth factor (VEGF) has been shown to be a survival factor for renal tubular epithelial cells. In the present study, we investigated whether administration of VEGF ameliorates tubulointerstitial fibrosis in a mouse model of unilateral ureteral obstruction (UUO).

Methods: Thirty-six male CD-1 mice were randomly divided into three groups: sham-operation, UUO and UUO+VEGF group.

[Relationship between the effect of vascular endothelial growth factor on epithelial-mesenchymal transition of HK-2 cells and the expressions of bone morphogenetic protein-7 and inhibitor of DNA binding/differentiation].

Objective: To examine the relationship between effect of vascular endothelial growth factor (VEGF) on epithelial-myofibroblast transition (EMT) of HK-2 cells and changes in expressions of bone morphogenetic protein-7 (BMP-7) and inhibitor of DNA binding/differentiation (Id) 2, Id3.

Methods: The cultured HK-2 cells were co-treated with transforming growth factor-beta1 (TGF-beta1) (5 ng/ml) and VEGF165 (0.1, 1, 10, 100 ng/ml), or with TGF-beta1 (5 ng/ml) and VEGF receptor-1 neutralized antibody (10 microg/ ml), and were also co-treated with TGF-beta1 (5 ng/ml) and VEGF165 (100 ng/ml) with or without activin receptor-like kinase 6 (Alk6)/Fc Chimera (2 microg/ml, to neutralize endogenous BMP-7) for 48 hours.

[The effects of mycophenolate mofetil on renal interstitial fibrosis and epithelial-myofibroblast translation in adenine-induced renal failure rats].

Objective: The aim of this study is to examine the effect of mycophenolate mofetil (MMF) on epithelial-myofibroblast translation (EMT) in adenine-induced chronic renal failure (CRF) rat model and the role of vascular endothelial growth factor(VEGF) and inhibitor of differentiation (Id2 and Id3) in EMT in the rat kidney.

Methods: Sixty-four male Wistar rats were randomly assigned to the following groups: normal control (n = 16), CRF (n = 24) and MMF(n = 24). CRF was induced by gastric gavage of adenine (125 mg kg(-1) d(-1)) to rats for eight weeks.

Inhibition of tubulointerstitial fibrosis by pentoxifylline is associated with improvement of vascular endothelial growth factor expression.

Aim: Recent information indicates that pentoxifylline (PTX) has the ability to suppress inflammation and profibrotic cell proliferation. In this study, we investigated the effect of PTX on tubulointerstitial fibrosis and the expression of vascular endothelial growth factor (VEGF) in a rat model of obstructive nephropathy.

Methods: Wistar rats with left ureteral ligation were divided into control and PTX-treated groups.

[Effects of induction of tubular epithelial-myofibroblast transition by monocyte chemoattractant protein-1 and mechanism thereof: an in vitro experiment].

Objective: To examine the effects of monocyte chemoattractant protein-1 (MCP-1) on epithelial-myofibroblast transition (EMT) of renal proximal tubular epithelial cells and the possible mechanism involved.

Methods: Human renal proximal tubular epithelial cells of the line HK-2 were cultured and divided into three groups: negative control group; positive control group, treated with transforming growth factor (TGF)-beta1 5 microg/L, and MPC-1 group, treated with MCP-1 0.1, 1, 10, and 100 microg/L for 24 h, 36 h, 48 h, and 72 h respectively.

[Effect of bone morphogenetic protein-7 on monocyte chemoattractant protein-1 induced epithelial-myofibroblast transition and TGF-beta1-Smad 3 signaling pathway of HKC cells].

Objective: To examine the effect of Bone Morphogenetic protein-7 (BMP-7) on Monocyte chemoattractant protein-1 (MCP-1) induced epithelial-myofibroblast transition (EMT) in cultured renal proximal tubular cells (HK-2) and the relationship between TGF-beta1-smad 3 expressions and MCP-1 induced EMT.

Methods: The cultured HK-2 cells were divided into six groups: a, negative control, b, treated with TGF-beta1 (5 ng/ml) as positive control, c, treated with MCP-1 (0.1, 1, 10, 50 ng/ml), d, treated with BMP-7 (0.

[Altered expression of vascular endothelial growth factor and its receptors in transdifferentiated human proximal tubular epithelial cells induced by transforming growth factor beta1].

Objective: To examine the expression of vascular endothelial growth factor (VEGF) and its receptors (VEGFR1, VEGFR2) in transdifferentiated human proximal tubular epithelial (HK-2) cell induced by transforming growth factor beta1 (TGFbeta1).

Methods: The transdifferentiation of HK-2 cells was detected by evaluation of expression of alpha-SMA by cytoimmunochemistry and RT-PCR. The VEGF mRNA was evaluated with RT-PCR.

[Effect of BMP-7 on the transdifferentiation of cultured human tubular epithelial cell induced by TGF-beta1].

Objective: To observe the effect of bone morphogenetic protein-7 (BMP-7) on the transdifferentiation of cultured human tubular epithelial cell (HKC) induced by TGF-beta1 and to elucidate its possible mechanism.

Methods: The cultured HKC cells were divided into 5 groups: serum-free group (negative control); single TGF-beta1 treated group (positive control); single BMP-7 treated group; combined TGF-beta1 and BMP-7 treated group; and BMP-7 pre-treated group. Expression of keratin of HKC cells was assessed by indirect enzyme immunohistochemistry (IEI), expression of alpha-smooth muscle actin (alpha-SMA) and E-cadherin by immunohistological method, percentage of alpha-SMA positive HKC cells by flow cytometry, and mRNA expression of alpha-SMA, TGF-beta1, and TGF-beta type II receptor by reverse transcription PCR.

[Expression of orexin A, orexin receptor-1, and Ob-R of hypothalamus in rats with chronic renal failure].

Objective: To examine the changes of expressions of orexin A, orexin receptor-1 (OX1R), prepro-orexin (Prepro-OX) mRNA, OX1R mRNA and ob-R of hypothalamus in rats with chronic renal failure (CRF).

Methods: Sixty-two male Wister rats weighing 200-250 g were divided into three groups, including group 1 (normal, n = 5), group 2 (sham-operated, n = 25) and group 3 (CRF, n = 32). Hypothalamus orexin A was assayed by radioimmunoassay.

[Phenotypic modulation of mesangial cells in diabetic rats and effect of tujian mixture].

Objective: To explore whether there is phenotypic modulation of mesangial cells in streptozotocin (STZ) induced diabetic rats and study the effect of Tujian Mixture (TJM) on it.

Methods: SD rats were divided into the normal control group (NC group, n = 8), the unilateral nephrectomized control group (QC group, n = 8), the STZ induced diabetes mellitus with unilateral nephrectomy model group (DM group, n = 8), the Valsartan treated group (VT group, n = 8) and the TJM treated group (ZY group, n = 9), rats in the latter two groups were modeled as in the DM group and treated with Valsartan (20 mg/kg.d) and TJM (20 g/kg.

[Orexin A and neuropeptide Y levels in plasma and hypothalamus of rats with chronic renal failure].

Objective: To explore the changes of orexin A and neuropeptide (NPY) in plasma and hypothalamus of rats with chronic renal failure (CRF).

Methods: 41 male Wister rats weighing 200 approximately 250 g were randomly divided into three groups: normal group, sham operation group, and CRF group (with the right kidney and 2/3 of the left kidney resected). A certain number of rats were decapitated 4, 8,and 12 weeks after respectively.

[Chinese herbs-induced renal failure with Fanconi syndrome: a report of 6 cases].

Objective: To understand the clinical and pathological features of patients with Fanconi syndrome associated with renal function damage induced by Chinese herbs.

Methods: Six cases with herb-induced renal failure associated with Fanconi syndrome were clinicopathologically analyzed.

Results: All six patients had kidney insufficiency after ingestion of Chinese herbs.