| Objective:The present study examined BDNF and its tyrosine kinase (Trk) receptors expression in a rat model of chronic CsA nephropathy, and the effect of vasopressin infusion on BDNF expression was also observed in vehicle and CsA-treated rat kidneys.Methods:Sprague-Dawley rats kept on a low salt diet (0.05% sodium) were treated daily for four weeks with vehicle (olive oil 1mL. kg-1, d-1 s.c.) or CsA (15mg. kg-1, d-1 s.c.).The expression of BDNF and TrkB and TrkC was evaluated with immunohistochemistry, immunofluorescence, and immunoblotting. In addition, urine concentration, histology, oxidative stress (8-hydroxy-2’-deoxyguanosine 8-OHdG), and apoptosis (TUNEL assay) were also compared for different treatment groups.Results:In VH-treated kidneys, BDNF and TrkB and TrkC were constitutively expressed in the collecting tubules of the outer medulla and cortex, which was confirmed by double immunofluorescence with BDNF and AQP-1 or AQP-2. CsA treatment increased urine excretion and this was accompanied by decreases in the expression of BDNF and TrkB and TrkC. The result of double immunofluorescencerevealed that BDNF and AQP2 were normally expressed in VH-treated kidney tissuesmainly located to collecting tubule cells, whereas their expression decreased significantly in the CsA-treated kidneys. DDAVP treatment preserved BDNF and AQP2 expression, which accompanied by decrease in urine volume [(9.2±1.5) ml vs. (22.7±2.4) ml,P<0.01].Conclusion:Ourobservations suggest that long-term treatment of CsA inhibits BDNF and its receptor expression in the kidney, and that this may be associated with impairment of urine concentration ability. Enhanced apoptotic cell death at least partially accounts for decreased BDNF and its receptor expression in a rat model of chronic CsA nephropathy. |
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