Effect of nitrotyrosine on renal expressions of NF-κB, MCP-1 and TGF-β1 in rats with diabetic nephropathy / 南方医科大学学报

<p><b>OBJECTIVE</b>To observe the effect of nitrotyrosine on renal expressions of nuclear factor-κB (NF-κB), monocyte chemoattractant protein-1 (MCP-1), and transforming growth factor-β1 (TGF-β1) in rats with diabetic nephropathy (DN).</p><p><b>METHODS</b>Rat DN models established by a single intraperitoneal injection of streptozotocin (STZ) were randomly allocated into model group, nitrotyrosine group and ebselen group, with untreated rats as the normal control group. The rats were given the corresponding drugs for 8 weeks, and after the last administration, the 24-h urinary protein level was measured and the kidneys of the rats were harvested for detecting the protein and mRNA expressions of NF-κB, MCP-1 and TGF-β1 with immunohistochemistry and RT-PCR, respectively. The pathological changes of the kidneys were assessed microscopically.</p><p><b>RESULTS</b>Compared with those in the model group, the 24-h urinary protein level and expressions of NF-κB, MCP-1 and TGF-β1 mRNA and protein in the renal tissues were significantly increased by nitrotyrosine treatment, which also caused worsened renal pathology, while treatment with ebselen significantly ameliorated these changes.</p><p><b>CONCLUSION</b>Nitrotyrosine can up-regulate the mRNA and protein expressions of NF-κB, MCP-1 and TGF-β1 and aggravate the inflammatory reaction in the renal tissue of DN rats to promote the progression of DN.</p>

Effects of Shenkangwan on renal expressions of angiotensin II and its type I receptor in rats with early diabetic nephropathy / 南方医科大学学报

<p><b>OBJECTIVE</b>To investigate the effects of Shenkangwan on the expressions of angiotensin II (AngII) and its type I receptor (AT(1)R) and the renalprotection mechanism of Shenkangwan in rats with early diabetic nephropathy (DN).</p><p><b>METHODS</b>The rat models of DN established by a single injection of streptozotocin were randomly divided into 4 groups, namely the model group, Shenkangwan treatment group, irbesartan treatment group, and Shenkangwan and irbesartan treatment group, with normal rats as the control. All the rats received daily gavage for 8 weeks. The urinary protein quality in 24 h and plasma and renal contents of AngII were measured. The expressions of AT1R at the protein and mRNA levels in the kidney tissues were measured by immunohistochemistry and reverse transcription-polymerase chain reaction, respectively. The pathological changes of the kidney were observed microscopically.</p><p><b>RESULTS</b>In DN rats, Shenkangwan reduced the urinary protein quantity in 24 h and the contents of AngII in the plasma and kidney tissues, decreased the renal expressions of AT(1)R protein and mRNA, and alleviated the morphological damage of the kidney.</p><p><b>CONCLUSIONS</b>Shenkangwan offers renalprotection against DN probably by reducing the contents of AngII in the plasma and kidney tissues and inhibiting renal AT(1)R expressions.</p>

Effects of angiotensin II receptor antagonist on rat podocyte injury in early diabetic nephropathy / 南方医科大学学报

<p><b>OBJECTIVE</b>To investigate nephrin and desmin expression in rat podocytes in early diabetic nephropathy (DN) and the rale of angiotensin II receptor antagonist in renal protection.</p><p><b>METHODS</b>Rat models of DN established by a injection of a single dose of streptozotocin (STZ) were randomized into model group and irbesartan group, with rats without STZ injection as the normal control group. The rats in irbesartan group were subjected to daily intragastric irbesartan administration for 8 consecutive weeks, while those in the model group received only saline in the same manner. Upon completion of the treatment, the rats were sacrificed and pathological changes of the kidney were examined with optical and transmission electron microscope. Nephrin and desmin expressions in the podocytes were detected by immunohistochemistry.</p><p><b>RESULTS</b>In rats with DN, irbesartan administration alleviated podocyte injury and significantly lowered the expression of nephrin and desmin (P<0.05).</p><p><b>CONCLUSION</b>Angiotensin II receptor antagonist may offer renal protection against DN by alleviating structural and functional podocyte damage through decreasing nephrin expression in the podocytes.</p>