Li-Ning Wang

Southern Medical University, Shengcheng, Guangdong, China

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Publications (19)29.75 Total impact

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    ABSTRACT: Vascular calcification is a risk factor for causing cardiovascular events and has a high prevalence among chronic kidney disease (CKD) patients. However, the molecular mechanism underlying this pathogenic process is still obscure. Vascular smooth muscle cells (VSMCs) were induced by a concentration of phosphorus (Pi) of 2.5 mM, and were subjected to cell calcification analyses. The effect of high Pi on the Wnt/β-catenin pathway was measured using a TOP/FOP-Flash reporter assay. The transcriptional regulation of β-catenin on PIT1 (a type III sodium-dependent phosphate cotransporter) was confirmed by promoter reporter and chromatin immunoprecipitation assays. The 5/6 nephrectomized rat was used as an in vivo model and was fed a high Pi diet to induce aortic calcification. Serum levels of phosphate, calcium, creatine, and blood urea nitrogen were measured, and abdominal aortic calcification was examined. High Pi induced VSMC calcification, downregulated expression levels of VSMC markers, and upregulated levels of osteogenic markers. High Pi activated the Wnt/β-catenin pathway and β-catenin activity. β-Catenin was involved in the process of high Pi-induced VSMC calcification. Further investigation revealed that β-catenin transcriptionally regulated Pit1, a necessary player in VSMC osteogenic phenotype change and calcification. The in vivo study showed that β-catenin was involved in rat abdominal aortic calcification induced by high Pi. When knockdown expression of β-catenin in the rat model was investigated, we found that aortic calcification was reduced. These results suggest that β-catenin is an important player in high phosphorus level-induced aortic calcification in CKD. © 2015 S. Karger AG, Basel.
    No preview · Article · Mar 2015 · American Journal of Nephrology
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    ABSTRACT: This study aimed to investigate the protective effect of metformin on renal injury of C57BL/6J mice treated with a high fat diet. High-fat diet for 12 weeks was used to establish the mice model of metabolism syndrome and the intervention of metformin (75 mg·kg-1 · d–1) for 4 weeks, and plasma biochemical indicator and body weight were used to evaluate the model. Sterol regulatory element-binding protein (SERBP)-1c, TNF-α, NADPH Oxidase (NOX)4 mRNA was determined by real time-PCR. Phospho-AMP-activated protein kinase (P-AMPK)α protein was detected by western blotting. Oil Red O staining, Masson staining and HE staining were for observing renal pathological changes. At the end of 12th week, compared with mice on low fat diet (LFD), body weight (BW), the levels of fasting insulin (FINS), plasma and renal triglyceride (TG) were higher and plasma high density lipoprotein (HDL) and insulin sensitivity index (ISI) were significantly lower, but the levels of fasting blood glycemia (FBG), plasma total cholesterol (TC) and renal TC had no changes; Oil Red O staining revealed renal lipids deposition, Masson staining and HE stain- ing revealed glomerular hypertrophy, matrix increasing, and inflammatory cells infiltration in glomerular; the expression of p-AMPKα protein decreased and the expression of SREBP-1c, TNF-α, NOX4 mRNA increased significantly in mouse treated with high fat diet (HFD). Compared with the HFD group, through metformin interventing, metabolic disorders were significantly improved, renal lipids deposition and other pathological changes were ameliorated, the expression of p-AMPKα protein increased and the expression of SREBP-1c, TNF-α, NOX4 mRNA decreased significantly. Metformin improved metabolic disorders, up-regulated activity of renal AMPK, diminished the expression of renal SREBP-1c, TNF-α, NOX4 mRNA, decreased accumulation of renal lipids, and prevened renal injury.
    No preview · Article · Dec 2014 · Pharmazie
  • Lin-lin Liu · Li-ning Wang · Yi Jiang · Li Yao · Li-ping Dong · Zi-long Li · Xiao-li Li
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    ABSTRACT: Background The efficacy of tonsillectomy in immunoglobulin A nephropathy (IgAN) remains controversial. Our meta-analysis was intended to investigate its efficacy as an adjunct or independent treatment. Study Design Meta-analysis of prospective and retrospective studies using PubMed, EMBASE, and the Cochrane Central Register of Controlled Trials. Setting & Population Patients with IgAN treated with or without tonsillectomy. Selection Criteria for Studies Studies that compared clinical remission or end-stage renal disease (ESRD) in patients with IgAN with or without tonsillectomy. Intervention Tonsillectomy. Outcomes Clinical remission and ESRD. Results 14 studies (1,794 patients) were included and a random-effects model was applied. There were significantly greater odds of clinical remission with tonsillectomy (10 studies, 1,431 patients; pooled OR, 3.40; 95% CI, 2.58-4.48; P < 0.001). Sensitivity analysis to exclude the effects of renin-angiotensin system inhibitors yielded consistent results (6 studies, 671 patients; pooled OR for remission, 2.80; 95% CI, 1.91-4.09; P < 0.001). In subgroup analysis of the remission outcome, tonsillectomy plus steroid pulse therapy was superior to steroid pulse therapy alone (7 studies, 783 patients; pooled OR, 3.15; 95% CI, 1.99-5.01; P < 0.001), and tonsillectomy plus conventional steroid therapy was superior to conventional steroid therapy alone (2 studies, 159 patients; pooled OR, 4.13; 95% CI, 1.23-13.94; P = 0.02). Tonsillectomy was superior to general treatment (3 studies, 187 patients; pooled OR for remission, 2.21; 95% CI, 1.20-4.05; P = 0.01). In addition, tonsillectomy was associated with decreased odds of ESRD (9 studies, 873 patients; pooled OR, 0.25; 95% CI, 0.12-0.52; P < 0.001). 2 sensitivity analyses, one excluding studies with less than 5 years’ follow-up and another excluding the confounding effect of renin-angiotensin system inhibitors, yielded nearly the same reduction in ESRD risk (6 studies, 691 patients; pooled OR, 0.20; 95% CI, 0.11-0.36; P < 0.001; and 6 studies, 547 patients; pooled OR, 0.24; 95% CI, 0.14-0.44; P < 0.001). Limitations Most included studies were retrospective cohort studies; we were unable to adjust uniformly for potential confounding variables. Conclusions As adjunct or independent therapy, tonsillectomy may induce clinical remission and reduce the rates of ESRD in patients with IgAN.
    No preview · Article · Oct 2014 · American Journal of Kidney Diseases
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    Li Sun · Quan Yuan · Ning Cao · Wei Guo · Li Yao · Jiang-Min Feng · Jian-Fei Ma · Li-Ning Wang
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    ABSTRACT: Objective: This meta-analysis aimed to investigate a comprehensive and reliable conclusion on the correlations of single nucleotide polymorphisms (SNPs) in the vascular endothelial growth factor (VEGF) gene with the risk of diabetic nephropathy (DN) in patients with diabetes mellitus (DM). Methods: We screened PubMed, Embase, Web of Science, Cochrane Library, CISCOM, CINAHL, Google Scholar, CBM, and CNKI databases for those relevant studies that investigated the association of 14,945 subjects with clinicopathological parameters in gastric cancer. Results: Eleven case-control studies that met all inclusion criteria were included in this meta-analysis. A total of 14,945 subjects were involved, including 3,049 DN patients and 11,896 DM patients. Our meta-analysis results revealed that VEGF rs2010963 and rs3025039 polymorphisms might contribute to the risk of DN in DM patients. Ethnicity-stratified analysis suggested that VEGF genetic polymorphisms were associated with an increased risk of DN among Asians. However, we found no correlations of VEGF genetic polymorphisms with susceptibility to DN among Caucasians. Conclusion: Our findings suggest that VEGF rs2010963 and rs3025039 polymorphisms may contribute to the risk of DN in DM patients, especially among Asians. Thus, VEGF genetic polymorphisms could be useful biomarkers for early diagnosis of DN in DM patients.
    Preview · Article · Aug 2014
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    ABSTRACT: Background/aims: The aim of our study was to reveal the role of CD44-Hyaluronic acid (HA) in the homing and improving renal function of systemically transplanted MSCs in chronic renal failure. Methods: First, a remnant kidney model was established in rats and the expression of HA was determined using immunohistochemistry (IHC) and western blotting. Next, chemotaxis assay using flow cytometry, and cell migration assay of MSCs were performed in vitro. Then, MSCs were transplanted into rats, thus, sprague-Dawley (SD) rats were randomly divided into sham group, 5/6 nephrectomy (5/6 Nx) group, MSC group and MSC/Anti-CD44 group (n = 8 for all groups). Migration of MSCs to the kidney in these rats was assessed by using cell tracking experiments, and tissue damage was evaluated by morphological analysis using Masson's trichrome staining and periodic acid Schiff staining. Results: HA was significantly observed in 5/6 Nx group, but not in sham group. Meanwhile, HA was discovered induced MSCs migration remarkably (p < 0.05) and anti-CD44 antibody inhibited the migration significantly (p < 0.05) in vitro. In vivo, the GFP-MSCs were observed in MSC group and the cells reduced in MSC/Anti-CD44 groups, especially, in the tubulointerstitium. Conclusion: Our findings reveal that CD44-HA has the potential to induce MSCs homing to injured tissue, while its effect on the ability of MSCs, improving tissue function, is not significant.
    No preview · Article · Jan 2014 · Kidney and Blood Pressure Research
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    ABSTRACT: There is accumulating evidence to support a hypothesis of the activation of the lectin complement pathway in IgAN. The glomerular deposition of mannose-binding lectin (MBL), an initiator of the lectin pathway, has been identified, but the clinical significance of it has not been defined consistently. The aim of the present study was to investigate the value of glomerular MBL deposition as a useful histological biomarker in evaluating the severity and predicting the prognosis of IgAN. We included all consecutive patients with biopsy-proven primary IgAN from December 2008 to July 2010. Renal deposition of MBL was detected by immunofluorescence. The biopsy material from 131 patients (72 men) was thus used for MBL staining. The deposition of MBL was observed in a predominantly mesangial pattern in 45 patients (34.35%), which presented as global or segmental deposition. Compared with the patients without glomerular MBL deposition, those with glomerular MBL deposition had more severe proteinuria, decreased renal function, lower levels of serum albumin and more possibility of hypertension at the time of renal biopsy; they had more severe histological changes according to the Oxford classification (i.e. mesangial hypercellularity, segmental glomerulosclerosis, endocapillary hypercellularity and tubular atrophy/interstitial fibrosis), and the ratio of them presented an increase as the histopathological phenotypes segregated according to Lee's classification; and furthermore, the follow-up data demonstrated that they had a lower renal remission rate. In conclusion, glomerular MBL deposition may predict a poor prognosis, and thus can be a new prognostic factor in IgA nephropathy.
    No preview · Article · Jun 2013 · Clinical & Experimental Immunology
  • Lin-Lin Liu · Yi Jiang · Li-Ning Wang · Li Yao · Zi-Long Li
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    ABSTRACT: Whether mycophenolate mofetil is superior to cyclophosphamide as induction therapy for lupus nephritis (LN) remains controversial. Our objective was to investigate the efficacy and safety of mycophenolate mofetil compared with cyclophosphamide as induction therapy for LN patients. Randomized controlled trials (RCTs) on humans were identified in searches of PubMed/MEDLINE, EMBASE and the Cochrane Central Register of Controlled Trials (all to 1 December 2011). Studies that compared the efficacy and safety between mycophenolate mofetil and cyclophosphamide as induction therapy in LN patients were selected. Methodological quality of the included trials was assessed according to Cochrane criteria and Preferred Reporting Items for Systematic reviews and Meta-Analyses (PRISMA) guidelines. The fixed effects model was applied for pooling where there was no significant heterogeneity, otherwise the random effects model (Dersimonian and Laird method) was performed. Results: Seven trials were identified, including 725 patients. The Dersimonian and Laird method was applied for renal remission in the presence of significant heterogeneity, and no statistically significant differences were distinguished between mycophenolate mofetil and cyclophosphamide. To explore the possible source of heterogeneity, meta-regression was performed. It was suggested that no obvious study- or patient-level factors could explain interstudy heterogeneity with statistical significance. Among all these factors, the mode of administration of cyclophosphamide could explain most of the heterogeneity, although the coefficient was insignificant. Therefore, we performed a sensitivity analysis by excluding the trial in which cyclophosphamide was administered orally instead of intravenously, which suggested that mycophenolate mofetil was more effective than intravenous cyclophosphamide for inducing complete remission (relative risk [RR] 1.72; 95% CI 1.17, 2.55; p = 0.006) and complete or partial remission (RR 1.18; 95% CI 1.04, 1.35; p = 0.01). In addition, mycophenolate mofetil was superior to cyclophosphamide for significantly reducing end-stage renal disease (ESRD) or death (RR 0.64; 95% CI 0.41, 0.98; p = 0.04). For the safety comparison, lower risks of leukopenia, amenorrhoea and alopecia, and a higher risk of diarrhoea were found with mycophenolate mofetil. No statistical differences in infection and gastrointestinal symptoms were distinguished between mycophenolate mofetil and cyclophosphamide. The relatively small number and the open-label fashion of eligible RCTs may limit the value of our meta-analysis. Mycophenolate mofetil is superior to intravenous cyclophosphamide for inducing renal remission, and has a significant advantage over cyclophosphamide for reducing ESRD or death. Furthermore, mycophenolate mofetil has lower risks of leukopenia, amenorrhoea and alopecia, but a higher risk of diarrhoea than cyclophosphamide. However, our conclusions need to be proved further in larger well designed trials.
    No preview · Article · Jul 2012 · Drugs
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    ABSTRACT: Background: To investigate the pathogenesis of diabetic nephropathy (DN) and to search for novel therapeutic targets, the glomerular protein expression profile of KKAy mice treated by losartan was analyzed by two-dimensional differential gel electrophoresis (2D-DIGE). Methods: The eight-week-old KKAy mice were divided into the losartan treatment group and the non-treatment group, and C57BL/6 mice were used as the control group. After 12 weeks treatment, glomeruli were isolated by abdominal perfusion with magnetic beads, and the glomerular proteins were extracted. The glomerular protein expression profiles were investigated using 2D-DIGE and MALDI-TOF mass spectrometry. Western blot analysis was used to confirm the results of proteomics. Results: Losartan treatment improved albuminuria and renal pathologic lesion of KKAy mice. A total of 62 glomerular proteins were differentially expressed between the KKAy losartan treatment mice and KKAy non-treatment mice. Among them, the expression of 28 proteins were up-regulated, including glycerokinase, sulfite oxidase, glycine amidinotransferase, and adenosylhomocysteinase. The expression of 13 proteins were down-regulated, including 3-mercaptopyruvate sulfurtransferase, ATP synthase subunit d, 60 kDa heat shock protein, and 75 kDa glucose-regulated protein(GRP75). A total of six proteins were found to be differentially expressed between the KKAy non-treatment mice and C57BL/6 mice glomeruli, and their differential expression was suppressed by losartan treatment, including mitochondrial ATP synthase subunit d, GRP75, and selenium-binding protein 1 et al. Conclusions: Treatment with losartan suppresses the differential expression of mitochondrial ATP synthase subunit d, GRP75, selenium-binding protein 1 etc. In diabetic KKAy mice glomeruli, may play a renoprotective role by reducing glomerular mitochondrial ROS genesis and inhibiting oxidative stress.
    No preview · Article · Jun 2012 · Journal of nephrology
  • Lin-Lin Liu · Li-Ning Wang
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    ABSTRACT: The efficacy of omega-3 fatty acids (O3FA) in IgA nephropathy remains a controversial issue. The aim of the current updated meta-analysis is to assess the efficacy of O3FA treatment for adult IgA nephropathy. We searched PubMed/MEDLINE, EMBASE and the Cochrane Central Register of Controlled Trials for randomized controlled trials that compared O3FA treatments with placebo or no treatment in adult IgA nephropathy. Outcomes of interest were effects on urine protein excretion (UPE) and renal function. Five RCTs (239 patients) were included for analysis. Compared with control groups, O3FA treatments did not show significant benefits for reducing UPE (standardized mean difference (SMD), -0.111; 95% confidence interval (CI), -0.369 - 0.147) or improving glomerular filtration rate (GFR) or estimated GFR (SMD, 0.177; 95% CI, -0.082 - 0.435), although the pooled results slightly favored O3FA. On the other hand, a lower risk of an increase of 50% or more in serum creatinine and ESRD were found in O3FA-treated IgA nephropathy patients (RR 0.189; 95% CI 0.068 - 0.524, p = 0.001; RR 0.236; 95% CI 0.094 - 0.594, p = 0.002), but the two outcomes were reported in only two trials. The current metaanalysis suggests that there are insufficient data to confirm the efficacy of O3FA treatments for proteinuria and renal function in IgA nephropathy. Further large scale trials are needed to shed more light on this issue.
    No preview · Article · Feb 2012 · Clinical nephrology
  • Lin-Lin Liu · Xiao-Li Li · Li-Ning Wang · Li Yao · Qiu-Ling Fan · Zi-Long Li
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    ABSTRACT: Systemic lupus erythematosus (SLE) associated with autoimmune thyroid disease (AITD) is a complex and well recognized autoimmune disorder. Careful monitoring/surveillance of thyroid gland functioning and active treatment of SLE patients with coexisting AITD, typically using medications, are critically important. The role of apheresis in this setting remains to be fully explored. Here we examine the use of double-filtration plasmapheresis (DFPP), as an adjuvant therapy in the treatment of patients with SLE complicated with AITD and report our experiences using this apheresis methodology. We performed a retrospective chart review of 11 patients with SLE complicated with AITD who had received DFPP in our blood purification center between 2004 and 2008. Levels of thyroid hormones, antithyroid autoantibodies, SLE disease activity, proteinuria, glomerular filtration rate (GFR), and response to therapy were analyzed. AITD, SLE, and lupus nephritis improved after DFPP. Except for one patient who died of severe pneumonia in the second month after completion of DFPP, all surviving patients continued to show clinical improvements or remained stable during the follow-up periods. DFPP can effectively remove autoantibodies and may have an important adjuvant role in therapeutic options in the treatment of SLE patients with AITD complications.
    No preview · Article · Jan 2011 · Journal of Clinical Apheresis
  • Lin-Lin Liu · Li-Ning Wang

    No preview · Article · Jan 2010 · Journal of Clinical Apheresis
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    Lin-Lin Liu · Mao-Ling Feng · Li-Ning Wang · Xiao-Li Li · Li Yao
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    ABSTRACT: Adult onset Still's disease (AOSD) is a rare systemic inflammatory disorder of unknown etiology and pathogenesis. The disease is characterized by typical spiking fever with evanescent rash, sore throat, polyarthralgias or polyarthritis, and involvement of various organs. Most of the reported cases with liver involvement occurred during the period of treatment with hepatotoxic drugs, whereas AOSD associated autoimmune hepatitis (AIH) is extremely rare. AIH may be an indicator of the poor prognosis of AOSD. Herein we describe a case of successful treatment with plasma exchange for AOSD-associated AIH.
    Preview · Article · Jan 2010 · Journal of Clinical Apheresis
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    ABSTRACT: The modifier protein (MP) of glyceraldehyde-3-phosphate dehydrogenase has been shown to promote growth of renal epithelial cells in vitro. The aim of this study was to show the in vivo effects of MP in a rat model of gentamicin-induced acute kidney injury (AKI). MP was purified from monkey renal tubular epithelial cell line BSC-1 and confirmed by amino acid sequencing. Male Sprague-Dawley rats were divided into the following groups: normal control, gentamicin-treated, epidermal growth factor (EGF) plus gentamicin-treated, and MP plus gentamicin-treated, as well as control groups for EGF and MP alone. Levels of serum creatinine (SCr), serum and tissue lipid peroxide, nitric oxide and glutathione-S-hydrogenase for each group were measured on the 7th and 14th days of treatment. Tissue sections were studied with light microscopy. The gentamicin-treated group showed a marked increase in SCr compared to the normal control group. Co-treatment of gentamicin with MP and/or EGF produced similar significant decreases preventing the increase in SCr. There were also significant reductions in serum and tissue homogenate levels of lipid peroxide and nitric oxide, accompanied by an increase in the level of glutathione-S-hydrogenase, in the MP co-treated groups compared to the gentamicin-treated group. AKI was confirmed histologically in the gentamicin-treated group, with damage to the tubular epithelium recorded. This was attenuated by MP co-treatment. There were also reductions in the expression of intercellular adhesion molecule-1 and proliferating cell nuclear antigen in the MP co-treated groups. Using a gentamicin model of AKI, MP was able to reduce free radical production in kidney tissue and in the circulation, thus preventing oxidant injury and minimizing damage in renal epithelial cells.
    No preview · Article · Nov 2009 · American Journal of Nephrology
  • Jie Zou · Jiang-Min Feng · Wei Li · Wei Guo · Li-Ning Wang
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    ABSTRACT: To investigate the potentiality of mesenchymal stem cells (MSCs) to differentiate into vascular endothelia cells (ECs) in peritubular capillary (PTC) in chronic aristolochic acid nephropathy (CAAN). MSCs were isolated from a male Wistar rat. The surface markers were identified with flow cytometry. Thirty female Wistar rats were randomly divided into 3 equal groups: Group A, perfused intragastrically with decoction of Caulis Aristolochiae manshuriensis for 12 weeks to establish CAAN models, Group B, perfused intragastrically with decoction of Caulis Aristolochiae manshuriensis for 12 weeks to establish CAAN models and injected with the MSCs by caudal vein in the 12th week, and Group C, perfused intragastrically with drinking water for 12 weeks and then injected with normal saline by caudal vein to be used as normal controls. At week 16, specimens of blood and urine were collected to detect the blood urea nitrogen (BUN), serum creatinine (Scr) and urine protein, and then the rats were killed with their kidneys taken out. Sex-determining region of the Y chromosome-fluorescence in situ hybridization (SRY-FISH) test with carboxyfluorescein (FAM)- was used to detect the cells originated from the source of the male donors. Immunohistochemistry was used to detect CD34, marker antigen pf EC. HE and Masson staining and electron microscope were used to observe the pathology of the kidney. Immunohistochemistry and RT-PCR were used to detect the expression of vascular endothelial growth factor (VEGF). Correlation analysis was conducted to study the relationships among these indices. Y chromosome and CD34 double positive cells could be seen in the renal tissue of Group B. At week 16, the density of PTC and integrated optical density of VEGF of Group A were (5.3 +/- 0.8)/0.13 mm2 and (2.8 +/- 0.4) x 10(3) respectively, both significantly lower than those of Group B [(26.5 +/- 1.6)/0.13 mm2 and (14.7 +/- 1.7) x 10(3) respectively, both P < 0.011]. The Scr and urine protein of Group A were significantly higher than those of Group B. The expression of VEGF mRNA of Group A was significantly lower than that of Group B. MSCs can differentiate into ECs. MSCs transplantation has beneficial effects on CAAN, which is possibly related with the reduction of PTC.
    No preview · Article · Mar 2008 · Zhonghua yi xue za zhi
  • Zhi-ming Li · Jian-fei Ma · Li-ning Wang
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    ABSTRACT: To investigate the influence of atorvastatin (ATOR) on the expression of monocyte chemoattractant protein-1 (MCP-1) induced by high concentration glucose in peritoneal mesothelial cells (PMCs) and the possible mechanism thereof. Rt PMCs were isolated, cultured, passaged, and divided into 3 groups: (1) treated with glucose of the concentrations of 0.1, 1.5, 2.5, 4.25% respectively, (2) treated with 1.5% glucose for 0, 0.5, 1, 3, 12, 24, and 48 h respectively, (3) pretreated with ammonium pyrrolidinedithiocarbomate (PDTC) of the concentrations of 5, 10, 25, or 50 micromol/L for 2 h, and then treated with 1.5% glucose for 3 h; and (4) pretreated with ATOR of the concentrations of 0.1, 1, or 10 mmol/L for 24 h, and then treated with 1.5% glucose for 3 h. Western blotting was used to measure the expression of MCP-1, p65, and inhibitor of nuclear factor-kappaBalpha (IkappaBalpha). RT-PCR was used to measure the expression of MCP-1 mRNA. PMCs expressed MCP-1 in the normal condition. Glucose dose- and time-dependently reduced the protein expression of IkappaBalpha in the PMCs and increased the p65 expression in the nucleus, and accelerated the PMCs to express MCP-1 mRNA and protein (P < 0.05 and P < 0.01). PDTC dose-dependently inhibited the acceleration of expression of MCP-1 mRNA and protein in the PMCs induced by high concentration glucose (P < 0.05 or P < 0.01). ATOR dose-dependently increased the IkappaBalpha expression, decreased the p65 expression in nucleus, and decreased the expression of MCP-1 mRNA and protein (P < 0.05 or P < 0.01). High concentration glucose induces PMCs to express MCP-1 in a time- and dose-dependent manner. Nuclear factor- kappaB (NF-kappaB) takes part in this regulation. ATOR inhibits PMCs to express MCP-1 through inhibiting NF-kappaB pathway.
    No preview · Article · Oct 2007 · Zhonghua yi xue za zhi
  • Zhi-Ming Li · Jian-Fei Ma · Li-Ning Wang
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    ABSTRACT: To investigate whether lipopolysaccharide (LPS) influence peritoneal mesothelial cells (PMCs) on their apoptosis, growth and expression of tumor necrosis factor (TNF) through IkappaBalpha, nuclear factor p65 pathway. PMCs were isolated, cultured and passaged by enzymatic disaggregation, then identified by phase contrast inverted microscope, transmission electron microscope and scanning electron microscope, with immunocytochemistry method. The PMCs were treated under conditions, which included different concentration LPS (normal control group, 0.1 mg/L, 1.0 mg/L, 10 mg/L, 50 mg/L, 100 mg/L) and different time (0, 1, 3, 6, 12, 24 hours). Hoechst 33258 fluorescence dye method was used to detect the apoptosis of PMC. The inhibitory effect of LPS on cell growth was measured with MTT method. Immunofluorescence dye was used to observe the activity of p65. Western blot method was used to detect the expression of IkappaBalpha. L929 cell line was used to detect the activity of TNF. RT-PCR was used to measure the expression of TNFalpha mRNA. LPS could inhibit growth of PMC and induce apoptosis. LPS could lead IkappaBalpha to degration and p65 into nucleus. LPS could also induce the expression of TNF. The expression of TNF-alpha mRNA reached the peak at the 1st hour and highest TNF activity at the 3rd hour. LPS inhibit the growth of PMC and induced the apoptosis. LPS induced PMC to express TNF-alpha in a dose-dependent manner. In the early state, PMC expressed a great deal of TNF-alpha, then began to fall quickly. During the period that LPS influence PMC on apoptosis, growth and expression of TNF, IkappaBalpha-NF-kappaB p65 pathway played the important role.
    No preview · Article · Apr 2007 · Xi bao yu fen zi mian yi xue za zhi = Chinese journal of cellular and molecular immunology
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    ABSTRACT: To investigate the effect of d-alpha-tocopherol on the expression of hexokinase (HK) induced by high glucose in cultured human peritoneal mesothelium cell (HPMC). Specimens of human omentum were obtained from consenting patient undergoing elective abdominal surgery. HPMC were isolated and subcultured by enzymatic disaggregation. Morphology and immunocytochemical method were used for identification. HPMC were divided into normal glucose group (0.1% glucose, equal to 5.5 mmol/L), high glucose group (0.5%, 1.0%, 1.5%, 2.5%, 4.25% glucose) and d-alpha-tocopherol group. After 24 h, standard G6PDH-coupled assay, temperature sensitive essay were used to detect the activity of total HK and its isozyme. Immunocytochemical staining was used for observation the intracellular location of HKII. Western blotting was used to analyze the protein expression of HKII and RT-PCR was used to detect the mRNA expression of HKII. The net glucose utilization was assayed by glucose disappearance from medium by hexokinase method. Primary cultured HPMC reacted positively for cytokeratin and vimentin and had numerous surface microvilli under electron microscope. High glucose induced HK activity in a dose-dependent manner and increased HKII isoform selectively. At concentration of 1.5%, 2.5% and 4.25% glucose for 24 h, the relative activity of total HK were 115.4%, 129.1% and 155.2%, respectively comparing with normal control (P < 0.05), and selectively increased HKII isoform expression. D-alpha-tocopherol blocked the activity of total HK and HKII induced by glucose. The relative activity of total HK inhibited by d-alpha-tocopherol was 82.1% (P = 0.001). After incubated with d-alpha-tocopherol, the net glucose utilization were decreased from (25.3 +/- 3.9) mmol/L to (17.3 +/- 2.1) mmol/L (P = 0.018). HKII stained light brown in cytoplasm of HPMC in normal group, accompanying with the increased concentration of glucose, the staining of HKII became strong and accumulated to nuclear. D-alpha-tocopherol made it thinning. The protein and mRNA expression of HKII were accorded with its activity. D-alpha-tocopherol inhibited the expression of HKII in activity, protein and mRNA induced by high glucose and decreased the net glucose utilization, which might become a method to improve ultrafiltration in peritoneal dialysis.
    No preview · Article · Aug 2006 · Zhonghua yi xue za zhi
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    ABSTRACT: To investigate the manifestation of impairment of peritubular capillary (PTC) in chronic aristolochic acid nephropathy (CAAN) and the influence of hypoxia caused by PTC impairment on the progression of CAAN. Fifty-four Wistar rats were randomly divided into 2 groups: Group A (n = 30, perfused intragastrically with decoction of Caulis aristolochia manchuriensis for 8 weeks) and Group B (n = 24, perfused intragastrically with drinking water for 8 weeks). At weeks 8, 12, and 16 ten rats in Group A and 8 rats in Group B were killed. Specimens of blood and urine were collected before the killing of the rats to detect the blood urea nitrogen (BUN), serum creatinine (Scr), and urine protein. HE and Masson staining and microscopy were used to observe the pathology of the kidney. Immunohistochemistry and Western blotting were used to detect the expression of hypoxia-inducible factor-1alpha (HIF-1alpha), vascular endothelial growth factor (VEGF), and CD34. Correlation analysis was conducted to study the relationships among these indices. Since week 8 BUN, Scr, and urine protein of Group A began to increase in comparison with Group B (all P < 0.05). Pathological changes of the kidney began to appear in Group A since week 8 with the decrease of PTC density. HIF-1alpha was not expressed in Group B, and in Group A HIF-1alpha expression began to increase since week 8 and became significantly higher than that of Group B since week 12. At week 16, the PTC density and VEGF-IOD of Group A were 8.10 +/- 2.28/0.13 mm(2) and (2.78 +/- 0.78) x 10(3) respectively, both significantly lower than those of Group B [(42.80 +/- 4.49)/0.13 mm(2) and (26.49 +/- 9.34) x 10(3) respectively, both P < 0.01], and the HIF-1alpha-IOD of Group A was (7.11 +/- 1.20) x 10(3), significantly higher than that of Group B [(0.44 +/- 0.10) x 10(3), P < 0.01]. CD34 was highly expressed in Group B, and the CD34 expression of Group A began to decrease since week 16. HIF-1alpha expression was positively correlated with Scr (r = -0.945, P < 0/01), and PTC density and VEGF expression were negatively correlated with Scr (r = -0.907, P < 0.01 and r = -0.690, P < 0.01). PTC density was negatively correlated with HIF-1alpha expression (r = -0.880, P < 0.01). Severe hypoxia exists following PTC injury in CAAN. Hypoxia is correlated with the progression of CAAN.
    No preview · Article · Jun 2006 · Zhonghua yi xue za zhi
  • Dong Sun · Jiang-min Feng · Yan-ling Zhao · Tao Jin · Li-ning Wang
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    ABSTRACT: To investigate the effects of prostaglandin E1 (PGE1) on the progression of aristolochic acid nephropathy (AAN). Twenty-four patients diagnosed as AAN with serum creatinine (Scr) between 1.5 mg/dL and 4 mg/dL during September 2001 to August 2003 were randomly divided into 2 groups. All patients had ingested long dan xie gan wan containing aristolochic acid (0.219 mg/g) for at least 3 months. Twelve patients were injected with Alprostadil (10 microg/d for 10 days in one month, summing up to 6 months). Except for PGE1, the other therapy was same in both groups. Renal function was assessed using reciprocal serum creatinine levels (1/Scr). The level of Scr an d serum hemoglobin (Hgb) was similar in both groups prior to therapy. During follow-up, 1/Scr levels in PGE1 group were significantly higher than control group (P < 0.01), and Hgb levels in PGE1 group were significantly increased compared with control (P < 0.05). PGE1 can slow the progression of renal failure and increase Hgb level of AAN patient.
    No preview · Article · Mar 2005 · Chinese Medical Sciences Journal

Publication Stats

61 Citations
29.75 Total Impact Points


  • 2015
    • Southern Medical University
      Shengcheng, Guangdong, China
  • 2010-2014
    • China Medical University (PRC)
      Feng-t’ien, Liaoning, China
  • 2007-2014
    • Guangzhou Medical University
      Feng-t’ien, Liaoning, China
  • 2008
    • ShenJing Hospital of China Medical University
      Feng-t’ien, Liaoning, China