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Objective To investigate the expression level and clinical significance of growth differentiation factor-15 (GDF-15) in type 2 diabetic nephropathy.Methods Sixty-eight patients (DN) of type 2 diabetic nephropathy treated in our hospital from January 2012 to 2013 January were chosen,in the same period,66 cases with type 2 diabetes mellitus (DM) and 30 cases normal volunteers without family history of diabetes in (NC) were studied as control in this study.Their blood routine and renal functions were detected.GDF-15 level was examined by enzyme linked immunosorbent assay (ELISA),receiver operating characteristic curve (ROC) curve was used to analyze the diagnostic significance of GDF-15 level.Results The level of GDF-15 in blood of patients with type 2 diabetic nephropathy was significantly higher than that in patients with type 2 diabetes and normal control group.GDF-15 levels was negatively correlated with low density lipoprotein (LDL),fasting insulin (INS) and glomerular filtration rate (eGFR) (P ＜ 0.05),and positively correlated with cholesterol (TC),triglyceride (TG),high density lipoprotein (HDL),fasting blood glucose (FBG),glycosylated hemoglobin (HbA1c),high-sensitivity C-reactive protein (hsCRP),creatinine (SCR),urea nitrogen (BUN),24 h urinary albumin (mAlb),and urinary albumin excretion rate (URER) (P ＜0.05).GDF-15 level had no correlation with body mass index (BMI),systolic blood pressure (SBP),and diastolic blood pressure (DBP) (P ＞ 0.05).GDF-15 levels could be used to diagnose type 2 diabetic nephropathy with 82.2％ sensitivity and 70.2％ specificity.Conclusions GDF-15 level has important significance in the diagnosis and pathogenesis of type 2 diabetic nephropathy.
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Objective To investigate the changes of CD4 + CD25 + Foxp3 + regulatory T cell (Treg) and relative cell factors in peripheral blood of steroid-resistant allergic rhinitis (AR) patients,and to study their functions in occurrence of steroid-resistant AR.Methods The CD4 + CD25 + Foxp3 + Treg cell in 30 cases general physical examination (The control group),30 cases steroid-sensitive AR patients (steroidsensitive group) and 30 cases steroid-resistant AR patients (steroid-resistant group) were detected by flow cytometry.The levels of serum interleukin 10 (IL-10) and transforming growth factor β1 (TGF-β1) in the three groups were detected by enzyme-linked immunoadsorbent assay (ELISA).Results Compare to the control group,proportion of CD4 + CD25 + Foxp3 + Treg cell and the levels of serum IL-10,TGF-β1 in steroid-sensitive group and steroid-resistant group were significantly reduced (P ＜ 0.01).The proportion of CD4 + CD25 + Foxp3 + Treg cell and the levels of serum IL-10,TGF-β1 in steroid-resistant group were decreased significantly than steroid-sensitive group (P ＜ 0.01).The proportion of CD4 + CD25 + Foxp3 + Treg cell were positively correlated with the serum IL-10,and TGF-β1 (P ＜ 0.01).Conclusions The reduced proportion of CD4 + CD25 + Foxp3 + Treg cell and lower serum IL-10,TGF-β1 play an important role in the occurrence of steroid-resistant AR patients.
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Objective To explore the role of transforming growth factor-β1/serum and glucocorticoid induced kinase 1 (TGF-β1/SGK1) signaling pathway in diabetic nephropathy (DN).Methods Totally 60 clean grade healthy male Sprague-Dawley (SD) rats were divided into normal control (Con group,n =20) and diabetic model group (diabetic group,n =40).Type 2 diabetic animal model was induced by intraperitoneal injection of streptozotocin (STZ,45 mg/kg) to SD rats.Half of rats in each group were sacrificed after implemented for 4 weeks and 8 weeks,respectively.Fasting glucose,serum urea and creatinine,as well as urine protein in 24 h were detected.Pathological changes of rats' kidney cortex tissue were examined by hematoxylin-eosin staining.The expression of SGK1 was detected by immunohistochemistry in renal tissue.The mRNA level of SGK1 was analyzed by real-time polymerase chain reaction (PCR).The protein expression of TGF-β1 and SGK1 were determined by Western blotting.Results Compared to the control group,the blood glucose of the diabetic group rats was significantly increased,kidney hypertrophy index,serum urea and creatinine,24 h urine volume and urinary microalbumin as well as kidney index were significantly higher (P ＜0.05).The mRNA expressed of SGK1,protein expression of TGF-β1 and SGK1 were also increased obviously in the renal cortex of diabetic rats (all P ＜ 0.05 vs Control).Conclusions TGF-β1/SGK1 signaling pathway is closely related to the TIF damage of kidney cortex in diabetic rats.
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Objective To explore the mechanism of diabetic hepatic fibrosis by observing effects of high glucose and insulin on expressions of transforming growth factor beta 1 (TGF-β1) and tissue inhibitor of metalloproteinase (TIMP-1) mRNAs of hepatic stellate cell (HSC) in rat.Methods Hepatic stellate cell lines in vitro were administrated by different dose of glucose without insulin and glucose with insulin for 72 h,and mannitol was chosen as hyperosmosis control group.Real time fluorescent quantitation polymerase chain reaction (RT-FQ-PCR) was used to determine expressions of TGF-β1 and TIMP-1 mRNAs of HSC in each group.Results Expressions of TGF-β1 and TIMP-1 mRNAs of HSC in each group could be detected and showed no significant difference among groups (P ＞ 0.05).However,in general,expression of TGF-β1 mRNA in glucose with insulin group decreased and TIMP-1 mRNA increased.Conclusions The mRNA expressions of TGF-β1 and TIMP-1 in HSC could not be induced by high glucose alone,high dose of insulin may increase expressions of HSC TIMP-1 and reduce TGF-β1 expression.The main mechanisms of diabetic hepatic fibrosis may not be TGF-β1 pathway but be closely related to TIMP-1 pathway.
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Objective To investigate the concentration change of indoxyl sulfate (IS) in blood and the renal expression of renal fibrosis-related factors (transforming growth factor-beta 1, TGF-β1;fibronectin, FN) after administration of mutagenic lactobacilli by oral.Methods A total of 60 male Sprague-Dawley (SD) rats aged 6 weeks was divided randomly into 3 groups.The normal control group (Sham group, n =20) received Sham operation of just incision of skin without kidney removed.The other two groups of rats were renal failure models selected from survivals of the other 40 rats who received real operation with 5/6 of kidney removed.Finally, 35 survived renal-failure rats were divided randomly into 2 groups : pathological control group(Model group, n =17) who were administrated of 2ml sterile saline solution once a day by gavage, and experimental group (lactobacillus bulgaricus (LB) group, n =18) who were administrated of 2 ml mutagenic lactobacilli (1.5 × 108 cfu/ml) once a day by gavage.Eight weeks later, blood specimens were taken to test the concentration of IS with high performance liquid chromatography-fluorescence detection (HPLC-FLU), and urea and creatinine by automatic biochemical analyzer;moreover, the rats were killed to get kidney tissues for pathological examination.Results The levels of serum IS, urea, and creatinine were statistically significantly different between two groups (P ＜ 0.05).Both the levels of renal tubular damage and renal interstitial fibrosis were both lessen in the experimental group compared to the model group (P ＜0.05).TGF-β1 and FN expressions in renal tissues were significantly decreased (P ＜0.05).Conclusions Mutagenic lactobacilli not only reduces serum concentration of IS, urea and creatinine in renal failure rats but lowers the expressions of TGF-β1 and FN in renal tissues.
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f fibrosis-related factors in LX-2cells were significantly increased after co-cultured with QSG7701-HBx cells, which proved that HBx could induce fibrogenesis in vitro.
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Objective To explore the role of TGF-βand TGIF in the pathogenesis of endometriosis. Methods The expression of TGF-β and TGIF was detected by immunohistochemistry method in the ectopic and eutopic endometrium of 30 cases with endometriosis (ec-topic endometrium group and eutopic endometrium group) and in the normal endometrium of 40 cases without endometriosis (control group). Result The expression of TGF -β in ectopic endometrium group was significantly higher than that in eutopic endometrium group and control group (P < 0.05). There was no significant difference in the expression of TGF- βbetween eutopic endometrium group and control group(P > 0.05). The expression of TGIF in ectopic endometrium group was significantly lower than that in eutopic endometrium group and control group( P <0.05). There was no significant difference in the expression of TGIF between eutopic endometrium group and control group(P > 0.05). There were negative correlation between the expressions of TGF - β and TGIF in ectopic endometrium group and eutopic endome-trium group(rs= - 0.769, - 0.549, P < 0.05). Conclusion The abnormal expression of TGF-β and TGIF in ectopic endometrium of pa-tients with endometriosis may be associated with the genesis and progression of endometriosis.