NIV Congres
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Donor pre-treatment with the heat shock protein-inducer geranylgeranylacetone reduces brain death-associated inflammation in the kidney at organ retrieval
Dullemen, L.F.A. van, Hoeksma, D., Ottens, P.J., Veldhuis, S., Ploeg, R.J., Leuvenink, H.G. D.
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Brain dead-derived kidney grafts have inferior transplantation outcomes compared to living donated kidneys. The protective heat shock proteins (HSP) are known to be up-regulated, but at the end of the brain death period. To reduce the brain death-related kidney injury, we want to increase the Hsp72 expression at the start of brain death. We investigated whether geranylgeranylacetone (GGA), an Hsp72 inducer, can reduce the pro-inflammatory changes and improve kidney donor quality in an in vivo brain death rat model.
Male F344 rats (275-300g, n=15) underwent slow induction of brain death and were kept brain dead for 4 hours. We administered GGA (400 mg/kg orally) or a saline vehicle 20h and 1h prior to brain death induction. Sham-operated animals (n=14) received the same treatment.
At the moment of organ retrieval, the expression of Hsp72 is not increased by GGA. However, kidney interleukin-6 mRNA levels in GGA pre-treated brain dead rats were lower compared to saline-treated controls. Systemic ASAT levels were also reduced by GGA, indicating decreased inflammation.
These results suggest that GGA reduces pro-inflammation during the brain death period, despite the unchanged expression of Hsp72. To further explore the effects of GGA on HSP expression, we want to assess expression of HSF-1 and other stress-induced HSP: Hsp90, Hsp32.
- Over Dullemen, L.F.A. van
- Over Hoeksma, D.
- Over Ottens, P.J.
- Over Veldhuis, S.
- Over Ploeg, R.J.
- Over Leuvenink, H.G. D.