Objective To investigate the renoprotective effect of erythropoietin(EPO) in streptozotocin-induced diabetic rats and to explore the possible mechanism.Methods The SD rats were randomly divided into there groups: normal control rats, diabetic, diabetic treated with EPO(NC, DM, DE groups).The rats were sacrificed after 8 weeks treatment.Renal morphology was observed by light microscopy.The expression of erythropoietin receptor(EPOR) in kidney was detected by immunofluorescence and Western blotting.The expression of p47phox, transforming growthfactor (TGF)β1andfibronectin (FN)proteininkidneywasdetectedby immunohistochemistry and Western blotting.The activity of antioxidants including total antioxidant capacity (T-AOC), superoxide dismutase (SOD), glutathione peroxidase (GSH-Px) and the level of malondialdehyde(MDA) in kidney were also measured.Results EPO treatment notably attenuated renal pathologic and functional changes.The expression of EPOR was found in kidney,but there was no difference among groups(P＞0.05).Compared with normal rats, diabetic rats showed an elevated expression of p47phox, TGF-β1, FN proteins and MDA levels in kidney as well as reduced activities of SOD, GSH-Px and T-AOC (all P＜0.01).Compared with diabetic rats, EPO could decrease the protein expression of p47phox,TGF-β1and FN in kidney (all P＜0.05).Meanwhile, elevated MDA level in the kidney was decreased as well as decreased SOD, GSH-Px,T-AOC activities were significantly remitted in DE group(all P＜0.01).Conclusion EPO can amelioraterenaldamagevia theinhibition of oxidativestressandTGF-β1andFNprotein expression in streptozotocin-induced diabetic rats.

Objective To investigate whether erythropoietin (EPO) can inhibit the proapoptotic effect of high glucose on rat proximal tubular epithelial cells, and the possible mechanisms in which EPO exerts its anti-apoptotic role. Methods Rat proximal tubular epithelial cells (NRK-52E) were divided into 5 groups: normal control group, osmolarity control group, high glucose group, high glucose with EPO (50 U/ml) group and high glucose with EPO (100 U/ml) group. The expression of EPO receptor (EPOR) in NRK-52E cells was examined by immunocytochemistry. The effect of high glucose on the expression of EPOR was detected by Western blotting. The rate of apoptosis was evaluated by flow cytometry Annexin V-FITC/PI double stains. The intracellular ROS was detected using fluorescent probe CM-H2DCFDA. The expression of bcl-2, bax and caspase-3 mRNA were examined by RT-PCR. Results The expression of EPOR was demonstrated in NRK-52E cells, and high glucose could up-regulate the expression of EPOR. High glucose could induce oxidative stress in NRK-52E cells, and up-regulate the mRNA expression of bax and caspase-3, down-regulate the mRNA expression of bcl-2. These effects of high glucose on NRK-52E cells could be reversed by EPO. Conclusion EPO inhibits NRK-52E cells apoptosis induced by high glucose through attenuating oxidative stress,up-regulating theexpression of bcl-2 mRNA and down-regulating the expression of bax and caspase-3 mRNA, which may be mediated by EPOR.

To investigate the gene mutation in a pedigree with X-linked ichthyosis (XLI) and to explore the relationship between the mutation and its clinical manifestations, genomic DNA of affected members, the normal member of the pedigree and 50 unrelated normal members was extracted with a whole blood genomic DNA extraction kit and the DNA was used as a template for the polymerase chain reaction (PCR)-mediated amplification of exon 1 and exon 10 of the STS gene. hHb6 (human hair basic keratin) gene was used as the internal control. Our results showed that the STS gene was deleted in affected members in the pedigree with X-linked ichthyosis. The normal member of the pedigree and 50 unrelated normal members had no such deletion. The proband and his mother had products in the internal control after PCR amplification. The blank control had no product. It is concluded that deletion of the STS gene existed in this pedigree with X-linked ichthyosis, and it is responsible for the unique skin lesions of X-linked ichthyosis.
Gene Deletion ; Ichthyosis, X-Linked/*genetics ; Pedigree ; Steryl-Sulfatase/*genetics

To investigate the gene mutation in a pedigree with X-linked ichthyosis (XLI) and to explore the relationship between the mutation and its clinical manifestations, genomic DNA of affected members, the normal member of the pedigree and 50 unrelated normal members was extracted with a whole blood genomic DNA extraction kit and the DNA was used as a template for the polymerase chain reaction (PCR)-mediated amplification of exon 1 and exon 10 of the STS gene. hHb6 (human hair basic keratin) gene was used as the internal control. Our results showed that the STS gene was deleted in affected members in the pedigree with X-linked ichthyosis. The normal member of the pedigree and 50 unrelated normal members had no such deletion. The proband and his mother had products in the internal control after PCR amplification. The blank control had no product. It is concluded that deletion of the STS gene existed in this pedigree with X-linked ichthyosis, and it is responsible for the unique skin lesions of X-linked ichthyosis.