虚血再灌流腎におけるHeme Oxygenase-1（HO-1）の役割

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  • Protective Effect of Heme Oxygenase-1 (HO-1) on the Ischemic Reperfusion Kidney

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 The contribution of heme oxygenase-1 (HO-1) in ischemic renal injury is little known. To investigate the role of HO-1 in the kidney, we examined the role of HO-1 in the ischemic re-perfusion kidney and its functional significance of an induction of HO-1. 36 Wistar Kyoto rats (WKY) were divided into three groups as follows; group I: control group (c, n＝12), group II: Fe-protoporphyrin treated group (hemin, 40μg/kg, n＝12) which provided substrate for HO-1 and group III: tin-protoporphyrin treated group (Sn-PP, 40μg/kg, n＝12) which blocked HO-1 synthasis. Bilateral ischemic acute renal injury was produced in 36 WKY, using a micro bulldog clamp. Re-perfusion was started after thirty minutes occlusion. Blood was collected for measurements of creatinine (Cr), blood urea nitrogen (BUN), arginine vasopressin (AVP) and the components of the renin-angiotensin system; angiotensin I (Ang I), angiotensin II (Ang II), plasma renin activity (PRA), plasma aldosterone concentration (PAC). Urine volume and urinary excretion of sodium were measured. In addition, both glomerular filtration rate (GFR) and renal plasma flow (RPF) were measured using inulin clearance and para-amino hippurate carried out. The kidney was removed before occlusion and at 3, 6 and 24 hours after re-perfusion for staining of HO-1 and aquqporin-2 (AQP-2) with immunohistochemistry method and measurements of mRNA levels of HO-1, endothelial constitutive nitric oxide synthase (ecNOS), and AQP-2 with reverse-transcription polymerase chain reaction (RT-PCR). At 3 hours after re-perfusion, HO-1 activity was increased significantly and most pronounced in the tubules in the kidney. In Sn-PP, both GFR and RPF group were significantly decreased and the suppression of the expression of HO-1 mRNA was observed. On the contrary, hemin treatment induced a significant elevation of GFR and RPF and increases in the expression of HO-1. After 24 hours in Sn-PP treated group, the expression of AQP-2 was suppressed accompanied with the increase of urine volume. HO-1 plays a key role in RPF and GFR in re-perfusion kidney and moreover is linked to regulate the expression of AQP-2. From these data, we conclude that the induction of heme oxygenase is a protective response in re-perfusion kidney after renal ischemia.

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