Expression of TGF-β1 in Placenta of the Patients with Pregnancy-induced Hypertension and Its relationship with Serum VCAM-1

The expression of transforming growth factor-β1 (TGF-β1) in placental tissue of pregnancy-induced hypertension (PIH) and the relationship between the level of expression of TGF-β1 and the amount of vascular cell adhesion molecule-1 (VCAM-1) in serum was studied. Immunohistochemistry ABC was used to detect the expression and distribution of TGF-β1 in placental tissues in 40 PIH women and 20 normal pregnancy women. High resolution pathological image analysis system was used to determine the quality of TGF-β. The VCAM-1 in serum was examined by enzyme linked immunoabsorbent assay (ELISA). The results showed that TGF-β1 could be express in syncytiotrophoblast. The levels of TGF-β1 expression in placental tissues of the patients with moderate and severe PIH were significantly higher (P<0.05), while the serum VCAM-1 was significantly lower than in normal group (P<0.01). There was a significant positive correlation between the expression of the TGF-β1 in placental tissues and the serum VCAM-1 (r=0.969,P<0.01). It was concluded that the level of TGF-β1 expressin in PIH was increased and was positively correlated with the amount of serum VCAM-1, indicating that they might be involved in the pathogenesis of PIH.     

The Expression of PLF in Placenta in Pregnancy-Induced Hypertension and the Relationship between the PLF and Serum VCAM-1

Summary:To study the expression of placental isoferritin(PLF)in placental tissue of pregnancy-in-duced hypertension(PIH)and the relationship between the level of expression of PLF and theamount of vascular cell adhesion molecule-1(VCAM-1)in serum,immunohistochemical techniquewas used to detect the expression of PLF in placenta tissue in 45 PIH patients(PIH group)and 15normal pregnant women(normal group).High resolution pathological image analysis system(HPIAS-100)was employed to determine the quantity of PLF.The VCAM-1 in serum was exam-ined by enzyme linked immunoabsorbent assay(ELISA).The results showed that the levels of PLFexpressions in moderate and severe PIH patients were significantly lower than that of normal group(P<0.01).The serum VCAM-1 was significantly decreased in PIH group(1310±177ρ/mg/ml)than that of normal group(609±72ρ/ng/ml,P<0.01).The significant negative correlation exist-ed betweene the expression of PLF in placental tissue and the serum VACM-1(r=0.58,P<0.01).It was concluded     

Expression of Endothelial Nitric Oxide Synthase Traffic Inducer in the Placenta of Pregnancy Induced Hypertension

Endothelial nitric oxide synthase traffic induc-er(NOSTRIN),a58kD(1kD=0.9921ku)pro-tein with complete unknown function that was i-dentified using the yeast two-hybrid system byZi mmermannet al[1],and Zi mmermann demon-strated that NOSTRIN over-expression induced aprofound redistribution of eNOS fromthe plasmamembrane to vesicle-like structures matching theNOSTRIN pattern and at the same ti me led to asignificant inhibition of NO release[1].WhetherNOSTRIN do involve in the mechani…     

Effects of <Emphasis Type="Italic">Panax notoginoside</Emphasis> on the expression of TGF-β1 and Smad-7 in renal tissues of diabetic rats

In order to explore the effects of Panax notoginoside (PNS) on the expression of transforming growth factor β1 (TGF-β1) and Smad-7 in renal tissues of diabetes, a rat model of diabetic nephropathy was set up by intravenous injection of streptozotocin (STZ). Wistar rats were randomly divided into normal group, diabetic control group, group treated by PNS at low-dosage (PL), group treated by PNS at high-dosage (PH) and group treated by catopril (C), respectively. Fasting blood glucose (FBG), renal index, endogenous creatinine clearance rate (CCr) and urinary albumin (UAlb) in 24 h were examined after 6 weeks. Meanwhile, the expressions of TGF-β1 and Smad7 in renal tissues were immunohistochemically dectected. At the end of the sixth week, FBG, renal index, Ccr, UAlb were all elevated significantly in control group (P<0.01). The expression of TGF-β1 protein was increased while Smad7 protein decreased in renal tissue (P<0.01). However, the treatment with PNS reversed the aforementioned changes in renal tissues of diabetic rats. These results indicate that PNS possess a protective effect on the kidney of diabetic rats and it might protect kidney by inhibiting the expression of TGF-β1 protein and enhancing the expression of Smad7 protein.     

Influence of High Level TGF-β1 on Scleral Thickness

In order to explore the role of TGF-β1 in scleral remodeling and the possible mechanism,the influence of high level TGF-β1 on scleral thickness and the expression of MMP-2 and TIMP-2 was investigated in a TGF-β1 transgenic mouse model.Alb/TGF-β1(Cys223,225Ser) TGF-β1 transgenic mice were used as experimental subjects and non-transgenic littermates as controls.Plasma levels of TGF-β1 were determined by ELISA.TGF-β1,MMP-2 and TIMP-2 levels in sclera were detected by using Western blot.The thickness of posterior sclera was measured by computerized image analysis of a midsagittal section.Mean difference was analyzed with independent t-test.The results showed plasma levels of TGF-β1 in transgenic mice were 1.68 times as much as that in the controls(P<0.01).TGF-β1 levels in the sclera of transgenic mice were 2.68 times of the controls(P<0.01).Posterior scleral thickness in transgenic mice were significantly thicker than in the controls.There was no significant difference in the MMP-2 levels between transgenic mice and controls,but the TIMP-2 levels were increased significantly in transsgenic mice as compared with those in the controls.It was suggested that high levels of TGF-β1 in transgenic mice could result in the increased scleral thickness by inducing the expression of TIMP-2 to suppress the activity of MMP-2,finally inhibiting the degradation of collagen.     

Modulation of Matrix Metalloproteinase and TIMP-1 Expression by TGF-β1 in Cultured Human RPE Cells

Matrix metalloproteinases(MMPs)are a familyof zinc binding,calcium-dependent endopeptidases thatfunction by degrading extracellular matrix(ECM)components.The functional effects of these enzymesare in part controlled byinteractions withtissueinhibi-tors of metalloproteinases(TI MPs)acting as naturalMMPinhibitors.Aprecise balance between MMPandTI MPactivities may be i mportant for the integrity ofECMcomponents[1].It shows that the expression andactivity of MMPs could be regulated by va…     

Ginsenoside Rb1, a panoxadiol saponin against oxidative damage and renal interstitial fibrosis in rats with unilateral ureteral obstruction

Objective:To investigate the possible protective effect and mechanism of ginsenoside Rb1 against oxidative damage and renal interstitial fibrosis on rats with unilateral ureteral obstruction(UUO). Methods:In total,80 male rats were randomly divided into 4 groups,20 in each group:the sham operated group (SOR),UUO group,UUO with ginsenoside Rb1 treatment group(treated with intraperitoneal injection of 50 mg/ kg daily) and UUO with Losartan treatment group(as the positive control,treated with 20 mg/kg by ga...     

The role of TGF-β1 in mice hepatic fibrosis bySchistosomiasis Japonica

Summary To investigate the role of transforming growth factor-β₁ (TGF-β₁) in mice with hepatic fibrosis caused bySchistosomiasis Japonica, ELISA, VG staining and multimedia color hieroglyph quantitative analysis were used to study the change of the serum TGF-β₁, liver collagen fiber and reticular fiber in mice. The level of serum TGF-β₁ in experimental group was significantly higher than that in control group (P < 0. 01 orP < 0. 05) 8, 10, 12 weeks after infected by schistosomiasis. After infection, the level of liver collagen fiber and reticular fiber, and that of TGF -β₁ increased over time (P < 0. 01 orP < 0. 05). In mice infected bySchistosomiasis Japonica, the level of TGF-β₁ increased with prolongation of infection time, and with the increase of liver collagen fiber and reticular fiber. TGFβ₁ plays an important role of immunomodulation in hepatic fibrosis formation caused bySchistosomiasis Japonica.     

Protective effects of eplerenone on podocyte injury in adriamycin nephropathy rats

To investigate the protective effects of eplerenone on adriamycin-induced renal injury and the possible mechanisms involved,36 male Sprague-Dawley rats were randomly divided into control group,adriamycin nephropathy(AN) group and eplerenone-treated group(100 mg.kg-1.d-1 eplerenone).Blood pressure,24-h urinary protein,serum potassium,sodium and creatinine were measured 28 days after adriamycin injection(a single tail intravenous injection of 6.5 mg/kg adriamycin).The morphological changes of renal tissues were observed by light and electron microscopy.Immunohistochemistry and Western blotting were performed to examine the expression of TGF-β1 and desmin in renal cortex.The results showed that 28 days after adriamycin injection,there were no significant changes in the level of serum potassium,sodium,creatinine concentrations and blood pressure values in the rats of the three groups.Meanwhile,the 24-h proteinuria excretion in the AN group was significantly higher than that in the control group(P<0.01),but that in the eplerenone-treated group was substantially reduced when compared with that in the AN group(P<0.05).Mild mesangial cell proliferation and matrix expansion,diffuse deformation and confluence of foot processes in podocytes were found in the AN group.By contrast,rats in the eplerenone-treated group exhibited obvious attenuation of these morphological lesions.The protein expression of TGF-β1 and desmin in the AN group was markedly up-regulated in contrast to that in the control group(P<0.01),whereas that in the eplerenone-treated group was much lower than in the AN group(P<0.05).It was concluded that eplerenone may ameliorate the proteinuria and the development of pathological alteration in adriamycin-induced nephropathy presumably via the inhibition of cytokine release,and restore the morphology of podocytes independent of its blood pressure-lowing effects.     

Effect of TGF-β1 on the expression of IL-12, IL-15, IL-18, IL-4 and IL-10 in heart transplantation rejection in rats

Summary To investigate the effect of TGF-β1 on the expressions of IL-12, IL-15, IL-18, IL-4 and IL-10 in heart transplantation rejection in rats, a model of rat cervical heterotopic heart transplantation was set up and the model rats were randomly divided into three groups: control group, transplant group and TGF-β1 group. The mRNA expression levels of IL-12, IL-15, IL-18, IL-4 and IL-10 were determined by RT-PCR at the 5th day after the transplantation. The mRNA expression levels of IL-12, IL-15, IL-18 were increased obviously and those of IL-4, IL-10 were significantly decreased in the transplant group as compared with the control group (P<0.01). In the TGF-β1 group, the mRNA expression levels of IL-12, IL-15, IL-18 were significantly decreased and those of IL-4, IL-10 were significantly increased as compared with the transplant group (P<0.01). The immunosuppressive effect of TGF-β1 on heart transplantation rejection was related to its inhibition of the expressions of Th1-type cytokines (IL-12, IL-15, IL-18 etc) and its promotion of the expressions of Th2-tpye cytokines (IL-4, IL-10).