[Gene transfer-induced human heme oxygenase-1 over-expression protects kidney from ischemia-reperfusion injury in rats].

Objective To study the protection of gene transfer-induced human heme oxygenase-1over-expression against renal ischemia reperfusion injury in rats. Methods The model of kidney ischemiareperfusion injury was established with Sprague-Dawley rats. In the therapy group (n = 18) ,the left kidney was perfused and preserved with Ad-hHO-1 at 2. 5 × 109 pfu/1. 0 ml after flushed with 0 ～4 ℃ HC-A organ storage solution via donor renal aorta. The rats in control groups were perfused with 0. 9% saline solution ( n = 12) or the vector carrying no interest gene Ad-EGFP 2. 5 × 109 pfu/1. 0 ml ( n = 18 ) instead of AdhHO-1. BUN and Cr in serum were measured by slide chemical methods. The kidney samples of rats were harvested for assay of histology, immunohistochemistry and quantification of HO enzymatic activity.Apoptosis cells in the kidney were measured by TUNEL. Results Ad-hHO-1 via donor renal aorta could transfect renal cells of rats effectively, enzymatic activity of HO in treated group [(1.62 ± 0. 07 )nmol · mg- 1 · min- 1] is higher than in control groups treated with saline solution team [( 1.27 ± 0. 07 )nmol·mg-1 · min-1] and vector EGFP team[(1.22 ±0.06) nmol · mg-1 · min-1] (P＜0. 01).Immunohistochemically , we found that the rats treated with Ad-hHO-1 expressed hHO-1 in kidneys at a high level. Corresponding to this, the level of BUN and Cr, as well as the number of apoptosis cells, were decreased, and the damage in histology by HE staining was ameliorated. Conclusion Over-expression of human HO-1 can protect the kidney from ischemia/reperfusion injury in rats. Key words: Kidney transplantation;  Heme oxygenase-1;  Ischemia-reperfusion injury;  Gene therapy