Aim To investigate the effects of valsartan on the expression of TGF-?1 mRNA and the activation of p38 mitogen-activated protein kinase(p38MAPK),mitogen activated protein kinase kinasse3/6(MKK3/6)and cAMP response element-binding protein1(CREB1) in glomerular mesangial cells under high concentration of glucose.Methods High concentration glucose and valsartan were used to stimulate the cultured rat GMCs in vitro.The protein expressions of p38 MAPK,CREB1,p-p38 MAPK,p-MKK3/6 and p-CREB1 were observed by Western blot analysis.TGF-?1 and fibronectin(FN) mRNA were measured by reverse transcription and polymerase chain reaction(RT-PCR).The protein synthesis of FN and type Ⅳ collagen in the supernatants of the GMCs was detected by radioimmunoassay.Results Compared with low glucose control group,the expressions of p-p38 MAPK,p-MKK3/6,p-CREB1 protein,TGF-?1 and FN mRNA,FN and type Ⅳ collagen in the supernatants were significantly increased in GMCs under high concentration glucose medium.The expression levels of p-p38 MAPK,p-MKK3/6 and p-CREB1 were significantly lower in the valsartan group than those in the high concentration glucose group.So did the mRNA of TGF-?1 and FN.The concentration of FN and type Ⅳ collagen in the supernatants in the valsartan group was lower than that in the high concentration glucose control group.Conclusion Valsartan can inhibit over production of TGF-?1 and ECM proteins in GMCs under high concentration of glucose,partly by regulating the phosphorylation of p38 MAPK,MKK3/6 and CREB1.

Objective To explore the correlations between expression of miRNA-21 and PTEN and the invasion, metastasis of colorectal carcinoma.Methods The mRNA level of miRNA-21 and mRNA and protein levels of PTEN were assayed by real-time quantitative PCR and immunohistochemical methods respectively in 65 colorectal carcinoma specimen.Results The expression of miRNA-21 mRNA in cancer tissues was significantly higher than that in paracancerous tissues (t =3.50, P ＜ 0.05).Both mRNA and protein expressions of PTEN in tumor tissue were significantly lower than that in paracancerous tissues (t =7.35,t =12.23;P ＜ 0.05).Expression of miRNA-21 mRNA, PTEN mRNA and protein were obviously related with depth of invasion(F =18.36 ,F =17.26 ,F =12.83;P ＜ 0.05), Dukes stage (F =31.25, F =24.43, F =57.12;P ＜ 0.05) and lymph node metastasis (t =5.85, t =2.18, t =4.05;P ＜ 0.05), while it was not related to tumor differenciation and tumor location (F =7.39, t =4.62;F =7.78, t =1.29;F =5.14,t =1.37;P ＞ 0.05).Positive relation between miRNA-21 and PTEN in colorectal carcinoma was identified (r =-0.994, r =-0.927;P ＜ 0.05).Conclusion High expression of miRNA-21 and low expression of PTEN are both closely associated with invasion and metastasis of colorectal carcinoma.

After the services provided by medical academic libraries for the readers of universities, their campuses and affiliated hospitals through the double WeChat service modelsubscription number +service numberwere in-troduced with Library of Xinjiang Medical University as an example, the problems in constructing WeChat platform were summarized with suggestions put forward for their solution .

Objective To explore the expression of the Pendrin gene (SLC26A4) and protein in multinodular goiter.Methods Thyroid tissues were obtained from 40 multinodular goiter patients undergoing surgery while the control group were obtained from 40 nomal thyroid tissues.RT-PCR was used to test SLC26A4 gene while western blot and immunohistochemistry were used to test Pendrin protein expression and distribution.Results SLC26A4 mRNA expression in multinodular goiter tissue was significantly increased in comparison with normal nodular tissues (t=2.663,P=0.011).Pendrin protein expression in multinodular goiter group was higher than that in normal tissue (t=2.286,P=0.026).The immunohistochemistry results showed that the Pendrin protein in multinodular goiter was mainly located in cytoplasm.There was positive expression in 24 patients (60％) in multinodular goiter group,while it was in 14 patients (35％) in the normal control group.The difference was significant (X2=5.013,P=0.025).Pendrin protein mainly expressed in cytoplasm in multinodular goiter tissue while it was mainly in cytomembrane in the normal control group.Conclusion SLC26A4 mRNA and its coding protein Pendrin expression are increased in multinodular goiter group,and mainly located in cytoplasm,indicating that iodide transporter function may be damaged when multinodular goiter occurs.

Aim To investigate the time-dependent effect of insulin on the expression of SREBP-1(sterol regulatory element binding protein-1),FAS(fat acid synthase)and lipid droplet formation in HKC cells(human renal proximal tubular epithelial cells line).MethodsHKC cells were respectively treated with 100 nmol·L~(-1) insulin for 0,2,4,6,12 h and 24 h.The analysis of SREBP-1 and FAS mRNA was performed by RT-PCR and the expression of SREBP-1 protein was detected by Western blot and immunocytochemistry.Furthermore,Oil Red O staining was used to determine cellular lipid droplet formation.ResultsCompared with HKC cells of 0 h group,there was no difference of SREBP-1 and FAS mRNA in HKC cells of 2 h group.However,the expression of SREBP-1 and FAS mRNA was significantly increased in HKC cells of 4,6 h and 12 h group.Further,the most expression of SREBP-1 and FAS mRNA was at 6 h group and was respectively increased by 3.578 and 4.272 times compared with 0 h group.The results of Western blot showed that the precursor and mature segments of SREBP-1 protein in 4,6 h and 12 h group HKC cells were increased and those of 6 h group HKC cells were the highest and about 4.106 and 5.167 times than those of 0 h group HKC cells.Immunocytochemistry presented the result that SREBP-1 protein was located in the plasma and the expression of 4,6 h and 12 h group HKC cells was significantly higher than that of 0,2 h and 24 h group HKC cells.The result of Oil Red O staining showed that lipid droplet markedly deposited in 6 h group HKC cells,contrarily,no lipid droplet was found in HKC cells of other groups.ConclusionAbove results suggested that insulin up-regulated SREBP-1 and FAS in time-dependent manner that led to cellular lipid droplet deposit,which may play an important role in the pathogenesis of renal lipid accumulation in metabolism syndrome.

Purpose To investigate the role of SOCS3 on diabetic renal injury. Methods Male CD-1 mice were randomly divided into four groups:control group, diabetic group, empty plasmid vector transfection group and SOCS3 plasmid transfection group. The diabet-ic mice were induced by intraperitoneal injection of STZ at a dose of 150 mg/kg body weight. The mice of transfection group were re-ceived an injection of SOCS3 plasmid or empty vector at every 7 days thereafter. Specimens were collected at 12 week after STZ injec-tion. The morphological changes of tubular epithelial cells were observed by transmission electron microscope. RT-PCR and immuno-histochemistry were used to determine the mRNA and protein expression of CK18 and α-SMA. Western blotting analysis was used to determine the protein expression of SOCS3, p-STAT3, CK18 and α-SMA. Results SOCS3 overexpression in kidney down-regulated the levels of p-STAT3 andα-SMA but up-regulated the expression of CK18. Conclusion Overexpression of SOCS3 can ameliorate the tubular epithelial-mesenchymal transdifferentiation of diabetic mice via inhibiting the phosphorylation of STAT3.

Objective To investigate the correlation between NF-?B/COX-2 signal pathway and cell proliferation in diabetic nephropathy. Methods Uninephrectomized STZ-induced male Wister rats were used as animal model. Using immunohistochemistry to detect NF-?B and COX-2 protein expressions in diabetic kidneys at the 16th week. HKC were cultured separately in normal or high glucose medium for 24,48,72 h.The expression of NF-?B and COX-2 protein was detected by flow cytometry and the expression of PCNA was detected by immunocytochemical staining. Results 1 Volum of glomeruli, mesangial matrix, thickness of glomerular and tubular basement membrane increased in diabete group; 2 COX-2 were expressed in cytoplasm of tubules and glomeruli by immunohistochemistry. Compared with control group, the expression of COX-2 was higher; activated NF-?B expressed in nucli of both tubules and glomeruli, There was light stainings for in control group, while enhanced stainings were observed in DM, there was a positive correlation between NF-?B and COX-2.3 Compared with those in HKC cultured in the medium with normal level glucose, the stainings were strengthened for PCNA in HKC exposed to high glucose from 24 h. 4 By FCM, the expression of NF-?B and COX-2 in HKC cultured in high glucose medium was higherthan that in normal glucose medium; the expression of NF-?B and PCNA was positively correlated with the expression of COX-2. Conclusion Activating NF-?B and elevating the expression of COX-2 play an important role in regulating cell proliferation, which may be one of the injury mechanisms of the renal cells during diabetic nephropathy.

Objective:To investigate the effect of HMGB1 and TLR-4 in the renal injury of SLE.Methods:The level of HMGB1 in serum from 16 patients suffering from SLE without kidney damage,18 patient with lupus nephritis (LN),and 12 healthy individuals were measured by ELISA.The fresh PBMCs were isolated and the total RNA was extracted.Then the mRNA expression of HMGB1 was amplified by RT-PCR.Flow cytometric analysis(FCM) was performed to study cell surface markers and the expression of TLR-4.Results:RT-PCR and ELISA results showed that the expressions of mRNA and protein were higher in patients with LN than in SLE without kindey damage and healthy people.The expression of TLR-4 in CD14+ monocytes of patients with LN was higher either,while there were no significant changes in CD3+ T cells among LN,SLE and healthy control.Conclusion:PBMCs in patients with LN could synthesize and secrete HMGB1 initiatively,which are correlated with serum HMGB1 level.HMGB1 might play a role in autoimmunity of lupus nephritis partly by activation of monocytes through its binding to TLR-4.

Objective:To investigate the effects of TLR/STAT pathway in the proliferation of mesangial cell induced by HMGB1.Methods:Human mesangial cells were inoculated in the dose of 1?104 ml-1.After 24 h,cells were cultured with standard medium as control group or with medium supplement with 10 ?g/L human recombinant protein HMGB1 as trial group in vitro.Then the cells were collected in 6,12 and 24 h respectively,as well as control group cells.Immunocytochemical staining was adopted to examine the expressions of PCNA proteins on mesangial cells in different groups.Immunocytochemical staining and FCM were performed to detect the changes of TLR2 protein expression.STAT1 and STAT3 mRNA were examined by RT-PCR technique.Results:Immunocytochemical staining indicated that the mesangial cells could multiply after they were induced by human recombinant protein HMGB1.Immunocytochemical staining showed that the level of TLR2 protein in trial groups were higher than those in control groups.FCM indicated that HMGB1 could significantly up-regulate the expression of TLR2 protein time-dependently.The STAT1 and STAT3 mRNA in HMGB1 groups were higher than those in control groups.The expression of TLR2 protein was positively correlated with those of STAT1 and STAT mRNA respectively.The positive rate of PCNA was remarkably correlated with the expression of STAT1 and STAT3 mRNA.Conclusion:HMGB1 could activate STAT1/STAT3 through combining with its cell-surface receptor TLR2,which may play an important role in promoting the proliferation of mesangial cells and then damaging the renal of lupus nephritis.

Purpose To investigate the role of S3I-201 on tubular interstitial lesion in lupus nephritis.Methods MRt/MpJ mice were designated as the control group.MRL/lpr nice were randomly divided into LN group,S3I-201 group and DMSO group.The serum and 24 h-urine were collected to detect the serum creatinine,blood urea nitrogen and urine protein.Immunohistochemistry was used to detect the expression of FN.Western blotting analysis was used to determine the expression of E-cadherin,α-SMA,MCP-1,ICAM1,STAT3 and p-STAT3.Results Compared with the expression level in control group,the protein level of α-SMA,MCP-1,ICAM1 and FN were increased in renal tissue of MRL/lpr mice,while the expression of E-cadherin was markedly decreased.And the STAT3 was activated in renal tissue of MRL/lpr mice.The administration of S3I-201 could inhibite the activation of STAT3 and ameliorate the expression of E-cadherin,α-SMA,MCP-1,ICAM-1 and FN.Conclusion S3I-201 can relieve the tubular interstitial leison,which maybe concerned with the phosphorylation of STAT3.