Chinese Journal of Tissue Engineering Research ›› 2015, Vol. 19 ›› Issue (49): 8021-8025.doi: 10.3969/j.issn.2095-4344.2015.49.026

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Expression of nestin in renal tissue of rat models of adriamycin nephropathy and the intervention of mycophenolate mofetil

Pan Feng-qi1, Jiang Hong2   

  1. 1Department of Pediatrics, First Hospital of China Medical University, Shenyang 110001, Liaoning Province, China; 2Department of Pediatrics, Central Hospital Affiliated to Shenyang Medical College, Shenyang 110024, Liaoning Province, China
  • Received:2015-09-07 Online:2015-11-30 Published:2015-11-30
  • About author:Pan Feng-qi, Master, Attending physician, Department of Pediatrics, First Hospital of China Medical University, Shenyang 110001, Liaoning Province, China

Abstract:

BACKGROUND: Studies have shown that podocyte injury is an important mechanism to generate glomerular proteinuria. However, it is not yet fully understood regarding the modulation method by which cytoskeletal proteins in the podocyte can maintain the unique morphology of podocytes. The construction and remodeling of podocyte cytoskeleton has become an increasing area of interest in the research field of proteinuria mechanism.
OBJECTIVE: To establish rat models of minimal change adriamycin nephropathy, and detect the expression of nestin in rat renal tissue under the intervention of mycophenolate mofetil.
METHODS: Thirty-six male Wistar rats were included and randomly divided into nephropathy model, mycophenolate mofetil and normal groups (n=12). Rats in nephropathy model and mycophenolate mofetil groups were intravenously injected with adriamycin via the tail vein at one time to establish models. Rats in normal group were intravenously injected with the same amount of normal saline via the tail vein. On the next morning, rats in mycophenolate mofetil group were intragastrically administered 20 mg/kg mycophenolate mofetil, once per day. Rats in nephropathy model group and normal group were given the same amount of normal saline daily. Four rats from each group were sacrificed at 14, 21 and 28 days after modeling. The renal cortex was harvested and subjected to hematoxylin-eosin staining and immunohistochemical staining. The pathological changes of renal tissue were observed and nestin expression in renal tissue was detected.
 
RESULTS AND CONCLUSION: In the normal group, rat glomerular filtration membrane structure was complete and epithelial cell foot process was clear. In the nephropathy model group, glomerular epithelial cell foot processes were fused to a large extent, and basement membrane was normal. In the mycophenolate mofetil group, glomerular epithelial cell foot processes were partly fused, but the pathological changes were milder. Immunohistochemistry results showed that beginning from the 14th day of modeling, rat nestin expression in the nephropathy model and mycophenolate mofetil groups was significantly increased compared with the normal group (P < 0.05). Rat nestin expression in the mycophenolate mofetil group was significantly lower than that in the nephropathy model group (P < 0.05). These results suggest that after glomerular podocyte injury, nestin expression in podocyte increased, while the expression increased with the aggravation of the disease. Mycophenolate mofetil can alleviate podocyte injury, downregulate nestin expression, maintain the normal structure of podocytes, and thereby achieve the purpose of delaying kidney damage.
 

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