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Objective To observe he effects of new Tangshenkang on α-SMA and E-cadherin of human renal tubular epithelial cell HK-2 in high concentrations of glucose; To explore the mechanism of new Tangshenkang on the prevention and treatment of diabetic renal fibrosis. Methods The HK-2 cells were cultured and divided into control group, high glucose group, animal serum control group, new Tangshenkang low-, medium-, and high-dosage group. After medicine intervention, cell proliferation was tested by MTT assay, and contents of α-SMA and E-cadherin were observed by ELISA assay. Results Compared with control group, α-SMA of HK-2 cultured with high glucose was much notable, but the content of E-cadherin significantly decreased, with statistical significance (P<0.05). The content of α-SMA of HK-2 cultured with new Tangshenkang decreased, and the content of E-cadherin increased; cell proliferation was markedly inhibited in culture medium supernatant of HK-2 cells cultured with high glucose plus new Tangshenkang compared with only high glucose, with statistical significance. Conclusion New Tangshenkang can inhibit cell proliferation and epithelial-myofibroblast transdifferentiation of HK-2 cell induced by high glucose, and prevent the development of diabetic renal fibrosis to a certain extent.
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Objective;To explore the mechanism ofSimiaosan drug-containing serum on prevention and treatment of renal fibrosis.Methods Human renal tubular epithelial cells (HK-2) were divided into blank group, model group, control group, and drug-containing serum high dosage group, medium dosage group and low dosage group. The expressions of CTGF and BMP-7 were determined by real-time PCR assay and immunocytochemistry.Results After the HK-2 cell was induced by uric acid (UA), the expression of CTGF significantly increased (P<0.05), the expression of BMP-7 significantly decreased (P<0.05). After intervened bySimiaosan, the expression of CTGF significantly decreased (P<0.05), the expression of BMP-7 significantly increased (P<0.05) and present dosage dependent.Conclusion Reducing the expression of CTGF and up-regulation the expression of BMP-7 and controlling epithelial-myofibroblast transdifferentiation may be the mechanism ofSimiaosan on prevention and treatment of renal fibrosis.
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Objective To investigate the protective effects of Wnt-7a protein on renal interstitial fibrosis in mice of unilateral ureteral obstruction (UUO)model.Methods Eighteen male C57BL/6 mice were randomly divided into 3 groups:sham-operation group,the UUO model group and Wnt-7a treatment group.The body weight of mice was measured everyday.All the mice were sacrificed at thc seventh day after the operation.The left kidney was taken for histology evaluation and molecular biology assay.Masson's stain was performed as a main indicator of interstitial fibrosis.The expression of vimentin,α-smooth muscle actin,and E-adherin in renal tissue was detected by immunohistochemistry staining and the expression of α-smooth muscle actin and E-cadhe(nn) in renal tissue was detected by Western blotting.Results Compared with sham-operation group,body weight of the (,)odel group was significantly lower (P＜0.05),and the relative area of interstitial fibrosis was significantly larger (P＜0.05).Furthermore,the expression of vimentin and α-SMA was significantly up-regulated (P＜0.05),and the expression of E-cadherin was significantly down-regulated (P＜0.05).Compared with model group,all the above-mentioned abnormalities were restored to some extent and showed significant differences (P＜0.05) in Wnt-7a treatment group.Conclusion Wnt-7a protein can decrease the interstitial fibrosis by inhibiting epithelial to mesenchymal transition in UUO mice.
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Objective To evaluate the inhibiting effect of antisense vascular smooth muscle alpha adenovirus vector on tubular epithelial myofibroblast transdifferentiation induced by TGF-?1.Methods The pAdanti-?-SMA was constructed and identified.The ?-SMA expression in tubular epithelial cells(TEC) was detected by immunofluorescence and Western blot.Five groups were designed as control(A),TEC transfected by 2 ?l pAdanti-?-SMA(B),TEC induced by TGF-?1(C),TEC induced by TGF-?1 and transfected by 2 ?l pAdanti-?-SMA(D),TEC induced by TGF-?1 and transfected by 10 ?l pAdanti-?-SMA(E).Results The pAdanti-?-SMA was successfully constructed.The expression of ?-SMA in TEC induced by TGF-?1 was inhibited by pAdanti-?-SMA.Conclusion Tubular epithelial myofibroblast transdifferentiation can be inhibited by pAdanti-?-SMA.