Splenectomy protects the kidneys against ischemic reperfusion injury in the rat
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文摘

Background

Ischemic reperfusion (I/R) injury of the kidney is closely associated with delayed graft function, increased acute rejection, and late allograft dysfunction. Splenectomy reduced hepatic I/R injury by inhibiting leukocyte infiltration in the liver, release of TNF-¦Á, cell apoptosis, and expression of caspase-3. Thus, we investigated the effects of splenectomy on renal I/R injury in the rat.

Methods

Male Wistar rats were assigned to four groups: sham operation (sham group), sham operation + splenectomy (sham + SPLN group), right nephrectomy followed by clamping the left renal pedicle for 30 min (I/R 30 group), and I/R 30 + splenectomy (I/R 30 + SPLN group). Renal function was determined by measuring the concentration of blood urea nitrogen (BUN) and serum creatinine (S-Cr). The serum level of tumor necrosis factor-¦Á (TNF-¦Á) was measured as the marker for inflammation. Left kidneys were obtained 24 h after reperfusion. TUNEL assay was assessed for cell apoptosis. Spleens were obtained immediately (0-h group) and 3 h after reperfusion (3-h group). The removed spleens were histologically evaluated.

Results

The BUN and S-Cr levels were significantly lower in the I/R 30 + SPLN group than in the I/R 30 group (p < 0.05 for both). Apoptotic cells were significantly lower in the I/R 30 + SPLN group than in the I/R 30 group. The serum level of TNF-¦Á, which was increased after I/R, was significantly lower in the I/R 30 + SPLN group than in the I/R 30 group (p < 0.05). Spleen weights were significantly lower in the 3-h group than in the 0-h group (p < 0.05).

Conclusion

These results suggest that splenectomy reduces renal I/R injury, and this effect may occur by an anti-inflammatory pathway and inhibition of cell apoptosis.

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